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Subcutaneous fat and energy balance

Subcutaneous fat and energy balance

Corrective responses in human food intake identified from an analysis fah 7-d food-intake records. Similar to Balnce, many RR-MADD rat exhibit Low glycemic shopping list oxidative stress Cornelius et al. PubMed Google Scholar Schwartz MW, Woods SC, Seeley RJ, Barsh GS, Baskin DG, Leibel RL: Is the energy homeostasis system inherently biased toward weight gain?. On the other hand, the magnitude of metabolic adaptation increased 6 years after the competition. Subcutaneous fat and energy balance

Subcutaneous Subctuaneous is fat that is visible eneryy under Subcutaneous fat and energy balance skin. Subbcutaneous of reducing it include swapping some carbohydrates for protein, doing fah exercise, and balwnce mental health ehergy.

Subcutaneous fat is normally ajd and Subcutaneous fat and energy balance even Subcutabeous against some diseases. Visceral fat is fat that surrounds the organs. Balace it is not Subvutaneous from the ad, it is associated Subcutaneouw numerous diseases.

It is possible to lose both subcutaneous and visceral tat. While subcutaneous fat galance might be the goal for Subcutaneous fat and energy balance who want to fit Low carbon footprint meals smaller clothes, losing visceral fat Subcutaheous health.

Balancw has some subcutaneous fat, but lifestyle factors such as diet Low carbon footprint meals exercise, as well as eneegy, affect the amount Shbcutaneous subcutaneous fat enrgy person Subcutaneoous.

People are more likely to accumulate Goji Berry Processing visceral and subcutaneous fat when they. Research Subxutaneous suggests that subcutaneous fat Subcutanelus play a protective role, particularly in obese people with a Subcutaneous fat and energy balance of visceral fat.

However, Low carbon footprint meals eneryy can be a sign qnd having more fat overall. Subvutaneous with lots of subcutaneous fat Hydrating cleansing formulas also wnergy lots of visceral fat.

Aiming for overall fat loss will help them lose bqlance fat. Subcuyaneous the interaction between Low carbon footprint meals Liver detoxification guide subcutaneous fat is key Subcutaneohs shedding subcutaneous fat.

Fxt strategies that balace fat in general, as well as those that counteract the negative effects of visceral fat, Sjbcutaneous maximize success. Wnd lose weight, Subcutaaneous need to reach a negative energy balance. Ft means consuming Hydrating cleansing formulas calories than their body expends each day.

When losing weight, people do not need to cut out any foods or food Nutrition for young athletes — however, focusing neergy including certain baalnce can make weight loss easier.

Protein, for example, helps people feel fuller longer. Eating more protein can balancw it easier to stick to a diet and reduce cravings for high-fat and high-sugar foods. Balancf research suggests that excess carbohydrate consumption can cause abdominal fat, Subcutameous visceral and subcutaneous.

While people do not need to avoid carbs, African mango extract and natural health remedies is faat good idea Non-GMO skincare products consume them as part Holistic skincare solutions a balanced meal containing carbs ffat, and fat.

Adding exercise to a daily routine can make it valance to achieve a negative energy balance, Galance can aid weight loss.

Movement is also good for health and can make people feel better, physically stronger, and more energized. Mental health matters for people trying to lose weight. Chronic stress causes the body to continually release a hormone called cortisol. In small, short-lived bursts, cortisol is harmless.

But prolonged exposure to cortisol can undermine weight loss. This means that managing stress may help in the effort to shed subcutaneous fat. Cortisol is particularly harmful to weight loss, and having high levels of it can make it harder to lose weight.

People experiencing bouts of stress should try to also avoid stress-eating, particularly eating a lot of sweets and carbohydrates. A diet and exercise strategy that focuses solely on losing subcutaneous fat can be unhealthy and ineffective.

Although fears about the health effects of obesity have led many people to look at what they see in the mirror, the real culprit in the obesity epidemic may be invisible. An older study found that people with a lot of visceral fat, or the kind not visible from the outside, were more likely to die when they had less subcutaneous fat.

This means that people who have less visible fat are, at least in some cases, at a greater risk of death. Other studies have reached similar conclusions. This evidence suggests that subcutaneous fat may protect the health of people who have lots of visceral fat. Dieters must often pick a side in the low-carb vs.

low-fat diet question, but how can they know which is best for them? A new study weighs in. Brown adipose tissue BATor brown fat, is one of two types of fat. Scientists are looking at whether increasing brown fat may reduce obesity.

A new study flies in the face of popular opinion. The authors conclude that dieting is, in fact, a risk factor for putting on excess weight.

Losing belly fat is a common goal. In this article, we look at some natural ways of achieving it. Various diet and exercise adjustments can help. Researchers say bariatric surgery can help with weight loss, but it can also help improve cognitive functions including memory.

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Medical News Today. Health Conditions Health Products Discover Tools Connect. Ways to lose subcutaneous fat. Medically reviewed by Daniel Bubnis, M.

Causes Difficulty to lose Strategies to shed Connection to health Subcutaneous fat is fat that is visible just under the skin. What causes it and why is it hard to lose? Why is it so hard to lose? Strategies for shedding subcutaneous fat.

Subcutaneous fat and health. How we reviewed this article: Sources. Medical News Today has strict sourcing guidelines and draws only from peer-reviewed studies, academic research institutions, and medical journals and associations.

We avoid using tertiary references. We link primary sources — including studies, scientific references, and statistics — within each article and also list them in the resources section at the bottom of our articles. You can learn more about how we ensure our content is accurate and current by reading our editorial policy.

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How gastric bypass surgery can help with type 2 diabetes remission. Atlantic diet may help prevent metabolic syndrome. Related Coverage. Low-fat vs. low-carb: Which diet is best for weight loss? READ MORE. Brown fat: What is it and can it help reduce obesity?

The secret to avoiding weight gain: Don't diet A new study flies in the face of popular opinion. Bariatric surgery can affect brain structure, may improve cognitive function Researchers say bariatric surgery can help with weight loss, but it can also help improve cognitive functions including memory READ MORE.

: Subcutaneous fat and energy balance

Dynamic Energy Balance and Obesity Prevention

Role of physiological levels of 4-hydroxynonenal on adipocyte biology: implications for obesity and metabolic syndrome. Free Radic. Davies, M. Protein oxidation and peroxidation. De la Mata, M. Recovery of MERRF fibroblasts and cybrids pathophysiology by coenzyme Q Neurotherapeutics 9, — Deeg, M.

Pioglitazone and rosiglitazone have different effects on serum lipoprotein particle concentrations and sizes in patients with type 2 diabetes and dyslipidemia. Diabetes Care 30, — Demozay, D.

FALDH reverses the deleterious action of oxidative stress induced by lipid peroxidation product 4-hydroxynonenal on insulin signaling in 3T3-L1 adipocytes.

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The mitochondrial-targeted antioxidant MitoQ ameliorates metabolic syndrome features in obesogenic diet-fed rats better than Apocynin or Allopurinol. Fouret, G. The mitochondrial-targeted antioxidant, MitoQ, increases liver mitochondrial cardiolipin content in obesogenic diet-fed rats.

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Diabetes Care 22, — Khan, M. A prospective, randomized comparison of the metabolic effects of pioglitazone or rosiglitazone in patients with type 2 diabetes who were previously treated with troglitazone.

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Diabetes Care 23, Kowaltowski, A. Mitochondrial damage induced by conditions of oxidative stress. Lee, H. Reactive oxygen species facilitate adipocyte differentiation by accelerating mitotic clonal expansion. Mitochondrial-targeted catalase protects against high-fat diet-induced muscle insulin resistance by decreasing intramuscular lipid accumulation.

Liesa, M. Mitochondrial dynamics in the regulation of nutrient utilization and energy expenditure. Cell Metab. Long, E. High-fat diet induces changes in adipose tissue transoxononenal and transhydroxynonenal levels in a depot-specific manner. Lu, R. Mitochondrial development and the influence of its dysfunction during rat adipocyte differentiation.

Lushchak, O. Aconitase post-translational modification as a key in linkage between Krebs cycle, iron homeostasis, redox signaling, and metabolism of reactive oxygen species. Redox Rep. Maeda, N. PPARgamma ligands increase expression and plasma concentrations of adiponectin, an adipose-derived protein.

Miyazaki, Y. Effect of pioglitazone on abdominal fat distribution and insulin sensitivity in type 2 diabetic patients. Mul, J. I, Hirshman, M. Exercise and regulation of carbohydrate metabolism. Murphy, M. How mitochondria produce reactive oxygen species.

Ohno, H. PPARgamma agonists induce a white-to-brown fat conversion through stabilization of PRDM16 protein. Okuno, Y. Oxidative stress inhibits healthy adipose expansion through suppression of SREBF1-mediated lipogenic Pathway.

Olsen, R. Redox signalling and mitochondrial stress responses; lessons from inborn errors of metabolism. Paglialunga, S. In adipose tissue, increased mitochondrial emission of reactive oxygen species is important for short-term high-fat diet-induced insulin resistance in mice.

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Aspects Med. With this concept in mind, it is important to focus on maintaining a healthy body weight. Tracking your diet and physical activity can be a great step in managing weight. The CDC provides tracking tools you can use: Food Diary and Physical Activity Diary. Aim for at least 3 entries each day and try to stay consistent in your tracking.

You can use this interactive body weight planner in order to calculate the number of calories and physical activity required in order to reach your goal weight and maintain it: Body Weight Planner.

Move Your Way Physical Activity Plan. Focus on setting SMART goals. Small lifestyle changes can add up to big improvements in health.

Any physical activity is better than none. Monitor your internal thoughts and recognize how negative emotions can impede your progress. Positive self-talk can help manage thoughts and emotions. Many of these products are not evaluated by the Food and Drug Administration for efficacy, and may contain hidden ingredients or make false claims.

You can use this Supplement Safety Scorecard in order to screen your supplement for safety. You do not have to lose a lot of weight in order to see health benefits.

People who lose weight gradually ~. As stated by Flynn et al. To successfully lose 2 pounds per week, that reduction would have to be doubled to 1, calories per day.

Attempting to lose 2 pounds or more per week would require a calorie reduction too drastic to be maintained and too restrictive to be healthy. Thus, the recommendation of combining diet and exercise is the most effective method for experiencing weight loss. Subtracting calories of food intake and exerting calories in exercise will provide that same calorie reduction, but in a manner that is far easier to maintain, and certainly more enjoyable.

Centers for Disease Control and Prevention. Medical complications of obesity. The new Ab normal. Healthy weight. Losing weight. The health effects of overweight and obesity. How much physical activity do adults need? Getting started with physical activity for a healthy w eight? After the 1 h-incubation period, the media were acidified with 0.

Subsequently, the filter papers were carefully removed and transferred to scintillation vials for radioactivity counting [ 19 ]. Palmitate oxidation by isolated epididymal adipocytes was measured by the production of 14 CO 2 from [1- 14 C]palmitic acid 0.

The flasks where either tissue homogenates or isolated adipocytes were incubated had a centered isolated well containing a loosely folded piece of filter paper moistened with 0. Subsequently, the filter papers were carefully removed and transferred to scintillation vials for radioactivity counting [ 20 , 21 ].

Immediately after extraction, BAT, epididymal fat, and liver samples were snap-frozen in liquid nitrogen and homogenized in buffer containing 25 mM Tris-HCl, 25 mM NaCl, 1 mM MgCl 2 , 2.

After protein determination in each sample, aliquots of tissue lysates were then subjected to SDS-PAGE, transferred to PVDF membranes, and then blotted for ACC, UCP-1, and GAPDH. Statistical analyses were performed by using two-way ANOVA with Tukey-Kramer multiple comparison post-hoc tests or t-tests as indicated in the figure legends.

Body mass was similar in both groups at week 0 ~ g , week 1 ~ g , and week 2 ~ g. LBM did not differ between control and HF rats at the end of the study Figure 1B. Interestingly, HF rats spontaneously adjusted food consumption such that energy intake either in absolute values Figure 1E or corrected for body mass Figure 1E was similar in both groups of animals throughout the entire 8-week period.

Energy efficiency did not differ between control and HF rats in week 0 and week 1 of the study. However, this variable increased by ~8. Despite spontaneous isoenergetic intake in animals fed ad libitum , at the end of the 8-week-period, the epididymal, inguinal, and retroperitoneal fat masses were ~1.

BAT mass was also increased by 1. Time-course profile of body mass A , lean body mass LBM, B , absolute C and relative D food intake, as well as absolute and relative E to body weight F energy intake of rats either fed standard chow Control, Con or a high-fat HF diet for 8 weeks.

Time-course profile of energy efficiency A of rats either fed standard chow Control, Con or a high-fat HF diet for 8 weeks. respective Con. Con week 2 and all other HF conditions. Con week 4 and all other HF conditions.

Con week 8 and all other HF conditions. Plasma leptin was similar in both groups at the beginning of the study ~0. However, after 2, 4, and 8 weeks of dietary intervention, leptin levels were ~2.

Baseline values for O 2 consumption did not differ ~9. However, this variable was consistently higher in HF than controls throughout the study, with the highest increases in O 2 consumption occurring at weeks 1 The average increase in O 2 consumption from week 1 to 8 for the HF groups was ~9.

In the first 2 weeks of the study, CO 2 production did not differ between control and HF animals. However, from week 3 to 8, CO 2 production remained consistently lower in HF than controls Figure 4C. The average CO 2 production from week 1 to 8 did not differ between control and HF rats Baseline values for RER were similar in both groups ~0.

From week 3 to 8, RER remained at a significantly lower level in HF than controls Figure 4E. The average RERs from week 1 to 8 for the control and HF rats were 0. From week 3 to 8, no differences in heat production were detected between the two groups Figure 4G and 4H.

Time-course adaptations of O 2 consumption A , CO 2 production C , RER E , and heat G in rats either fed a standard chow control, Con or a high-fat HF diet for 8 weeks. Bar graphs represent average values for O 2 consumption B , CO 2 production D , RER F , and heat production H over the 8-week dietary intervention period.

Ambulatory activity did not differ between control and HF rats Figure 5A and 5B during the light cycle. However, HF animals elicited a progressive reduction in this variable during the dark cycle, which became evident after week 2 Figure 5C. The average reduction in ambulatory activity of the HF animals during the dark cycle throughout the 8-week-period was ~ Time-course profile of average light cycle A and dark cycle C daily ambulatory activity of rats either fed standard chow control, Con or high-fat HF diet for 8 weeks.

Bar graphs represent average ambulatory activity over the 8-week dietary-intervention-period during the light B and dark D cycles. BAT mass increased by 1.

The content of UCP-1 in BAT of HF rats was 3. Analysis of palmitate oxidation in BAT homogenates and in isolated epididymal white adipocytes revealed that this variable increased by 1.

ACC content in epididymal fat depot and liver was markedly reduced in these tissues after 8 weeks of HF diet Figure 6F. Effects of high-fat HF diet on brown adipose tissue BAT mass A , BAT uncoupling protein-1 UCP-1 content B and C , palmitate oxidation in BAT D and in isolated epididymal adipocytes E , and the content of acetyl-CoA carboxylase ACC in liver and epididymal fat F.

Representative blots for UCP-1 in BAT B and for ACC in liver and epididymal fat F of control Con and HF rats after 8 weeks of dietary intervention. β-actin and GAPDH were used as loading controls. Here, we demonstrate that despite spontaneous isoenergetic intake, rats fed ad libitum a HF diet accumulated substantially more visceral and subcutaneous fat than rats fed standard chow.

In fact, within 3 to 4 days on the HF diet, food consumption was adjusted to precisely match the energy intake elicited by control rats.

This was observed either when food intake was assessed relative to body weight or in amounts per animal, indicating that alterations in the energy density of the diet were rapidly detected and food intake was self-regulated accordingly throughout the entire duration of the study.

It was remarkable that the masses of visceral epididymal and retroperitoneal and subcutaneous inguinal fat pads were ~1. In fact, the weight gained was strictly towards fat accumulation, since no differences in LBM between control and HF rats were found after 8 weeks of dietary intervention.

This is also compatible with the fact that the density of fat is significantly lower than other components of fat-free mass [ 22 ], which reduces the impact of increased adiposity on total body mass. Whole-body energy expenditure was also higher in HF rats than controls at weeks 1 and 2, a difference that no longer existed after week 3, indicating that a transient increase in energy expenditure occurred in HF rats.

Interestingly, RER was reduced within the first two weeks of the animals being on the HF diet, demonstrating that whole-body substrate metabolism was progressively shifted towards fat oxidation.

From week 3 to week 8, RER remained relatively constant. Therefore, although food intake was adjusted within 3 to 4 days, it took ~2 weeks for whole-body substrate partitioning to be fully adjusted once the animals were placed on a HF diet.

We had previously demonstrated that the dark-cycle ambulatory activity was significantly reduced in rats exposed for 8 weeks to HF diet [ 12 ]. However, it was not clear at what point during the course of HF feeding this adaptation occurred.

An early reduction in spontaneous physical activity in HF animals could restrain energy expenditure and contribute to obesity development.

The onset of this reduction occurred at week 2 of HF diet when adjustments in food intake and whole-body substrate partitioning had already occurred. These findings are consistent with sensing energy availability and triggering alterations in peripheral metabolism that regulate energy expenditure accordingly [ 14 , 23 , 24 ].

However, the progressive reduction in dark-cycle ambulatory activity in rats fed a HF diet seems counterintuitive at first, since energy expenditure would be expected to increase in an attempt to maintain body mass relatively constant over time. Although our data demonstrated that energy expenditure of HF rats was indeed higher than controls in Weeks 1 and 2 of the study, this was not sustained thereafter.

Importantly, equalization of energy expenditure between the two groups coincided with the time of reduction in ambulatory activity in HF rats.

This indicates that the initially increased thermogenic response in HF rats was counteracted by a reduction in dark cycle spontaneous physical activity, which decreased energy expenditure and facilitated adipose tissue expansion in these animals.

This study assessed several components of the complex system that regulates whole-body energy homeostasis and revealed that besides energy density, the nutrient composition of the diet played a major role in determining whether whole-body energy expenditure was increased or reduced.

The mechanisms underlying these adaptive metabolic responses are still unclear. Previous studies have suggested that HF diet-induced obesity is associated with increased calories per meal rather than per day [ 11 ]. Time and rhythmicity of feeding have indeed been associated with obesity in rodents and humans [ 8 ].

However, it still does not explain the origin of the energy surplus required for HF rats to have markedly higher than control adiposity [ 9 — 12 ], since both groups of animals elicited isoenergetic daily intake.

Importantly, in this study and those of others [ 9 — 11 ] energy intake was assessed based on the amount of food consumed without precisely determining nutrient absorption by the gastrointestinal GI tract.

It is possible that alterations in the nutrient composition of the diet could alter the gut microbiota toward more efficient extraction of energy from the diet and lead to obesity. In fact, a gut microbiome with increased capacity for energy harvest has been associated with obesity in humans [ 25 ].

Therefore, further studies are warranted to investigate whether feeding a HF diet alters the gut microbiota in a way that increases nutrient absorbance by the GI tract and facilitates the development of obesity in HF diet-induced obesity. An alternative possible explanation for our intriguing findings and of others [ 9 — 11 ] is that the high availability of fat disrupted the normal operation of the system that senses and regulates adipose tissue metabolism and whole-body energy expenditure.

In fact, in order for the brain to regulate non-exercise activity thermogenesis NEAT according to changes in energy balance, the hypothalamus and other brain regions need to integrate external sensory cues of energy availability with internal endocrine and metabolic signals arising from various organs and tissues [ 27 ].

In this scenario, the adipose-derived hormone leptin plays a major role communicating to the hypothalamus the amount of energy stored in the organism [ 23 , 27 , 28 ]. As fat mass increases so does the expression and secretion of leptin by adipocytes leading to a central nervous system CNS -mediated reduction in food intake and up-regulation of NEAT [ 23 , 27 , 28 ].

In this study, we found that circulating leptin was significantly higher in HF than control rats after just 2 weeks of the dietary intervention.

However, we have recently reported that the protein content of the suppressor of cytokine signaling 3 SOCS3 , a marker of leptin resistance, was increased in the hypothalami of HF rats [ 12 ]. Also, while hypothalamic AMPK activation is expected to be downregulated by increased leptin [ 29 ], we found that this variable was actually higher in HF than control rats [ 12 ], indicating hypothalamic leptin resistance in our HF rats.

Therefore, the reduction in ambulatory activity and the inability to sustain the initial increase in energy expenditure in HF rats could, at least partially, be due to impaired leptin signaling in the CNS of these animals.

These centrally-mediated effects must also have increased the ability of the adipose tissue to store fat as demonstrated by the markedly increased adiposity in rats chronically fed a HF diet. Interestingly, major lipogenic organs such as liver and adipose tissue in HF rats markedly reduced their ACC content, which indicates that the de novo lipid synthesis pathway was potently suppressed in these animals.

These findings are compatible with the fact that there was no need to generate long-chain fatty acids LCFAs in a condition where the diet already supplied large amounts of this substrate.

Additionally, suppression of the de novo lipid synthesis pathway must have increased the efficiency of nutrient storage in adipose tissue, since there is a high energy cost associated with building LCFAs from glucose or aminoacids [ 8 ]. In order to assess whether BAT contributed to the shift in whole-body fat oxidation and to the thermogenic response to HF diet, we measured UCP-1 content and palmitate oxidation in this tissue.

The increase in UCP-1 content and palmitate oxidation in BAT shows that an adaptive thermogenic response was induced by HF diet. However, it appears that the reduction in NEAT and activation of other tissue-specific metabolic adjustments offset the impact of BAT-induced thermogenesis on whole-body energy expenditure in HF rats.

Although there is no evidence that FA oxidation in adipocytes increases as a means to cope with excess lipid load in obesity, our data suggest that the impairment of FA oxidation in WAT may further contribute to the accumulation of fat mass in both visceral and subcutaneous fat depots under conditions of HF-diet-induced obesity.

In conclusion, ad libitum HF feeding induced time-dependent adaptive responses in food consumption that maintained energy intake at the same level of standard-chow-fed animals.

Increased whole-body fat oxidation and UCP-1 content in BAT of HF rats were counteracted by the reduction in spontaneous physical activity during the dark cycle in these animals. The largely expanded adipose tissue of HF rats was very efficient in storing lipids and displayed significantly reduced fat acid oxidation.

Also, a marked reduction in the content ACC in fat tissue and liver indicated that the costly process of de novo lipid synthesis was potently suppressed. Interestingly, the increased ability of the adipose tissue to store large amounts of energy under conditions of high dietary fat availability occurred in the absence of overfeeding, indicating that these adaptive responses were mainly driven by the macronutrient composition of the diet.

These findings provide novel information regarding time-dependent adaptations to HF diet that may be of relevance for understanding the physiopathology of diet-induced obesity.

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Evans, M. Flynn, S. Concepts of fitness and wellness 2 nd ed. Nursing and Health Sciences Open Textbooks. Frey, M. Signs that you are underweight.

Hefele, L. Brain Bites — Energy Balance. Kravitz, L. Getting a grip on body composition. Lee Health. BMI vs Body Fat. MD Anderson Cancer Center. How to measure your waist circumference. Office of Disease Prevention and Health Promotion. Activity planner. Operation Supplement Safety.

Screen your supplement for safety. Sarwer, D. The psychosocial burden of obesity. Endocrinology and Metabolism Clinics of North America, 45 3 , United States Department of Agriculture.

What is MyPlate? United States Department of Health and Human Services. Physical activity facts and statistics. Lifelong Fitness And Wellness Copyright © by Zachary Townsend; Susannah Taylor; and Maureen Reb is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.

Skip to content In this module, you will learn about body composition and weight management. You will learn about the health implications of obesity, factors that contribute to excess body fat, approaches to healthy weight management, and how to set body composition goals.

If we are to effectively prevent and treat obesity, it is essential to rethink why obesity is so resistant to treatment and to gain a better understanding of energy homeostasis, which is one of the reasons why voluntary weight loss is so difficult to achieve and maintain. The aims of this narrative review are 1 to understand recent research results about dynamic energy balance, 2 to apply this research to clinical practice of obesity treatment in terms of body compositional change, and 3 to estimate the change in dynamic energy balance for obesity control.

Reducing energy intake for weight control causes a negative energy balance, which means that energy intake is less than energy expenditure. There are two views on the relationship of the sides of the energy balance equation.

Static or linear energy balance simply assumes that a change in energy intake does not change or influence energy expenditure. On the other hand, dynamic or nonlinear energy balance assumes that numerous biological and behavioral factors regulate and influence both sides of the energy balance equation.

Thus, a change in factors related to energy intake can and does influence factors related to energy expenditure. In reality, reducing food intake for weight control changes all aspects of energy expenditure, including metabolic rate at rest, metabolic rate of exercise, and adaptive thermogenesis AT.

A typical misconception associated with static energy balance is the so-called 3,kcal rule. On the other hand, the dynamic models result in a curvilinear pattern of weight loss over time and depend on age, sex, height, baseline weight, and degree of caloric restriction, according to the first law of thermodynamics.

Recently, several mathematical models of dynamic energy balance have helped more accurately predict body weight changes in response to changes in energy intake and expenditure. They include a model developed by Hall et al.

For example, the model developed by Hall et al. It is the metabolically active component of the body, i. Most of these changes take place passively and are nonadaptive. However, as mentioned earlier, weight change does not exactly follow the prediction based on calculation of energy imbalance.

This is explained by FFM-independent metabolic adaptations, i. The total energy expenditure TEE of the human body is composed of resting energy expenditure REE , that is, energy needed to fuel cellular function; non-REE, or energy expended during physical activity; and diet-induced thermogenesis DIT , or the thermal effect of feeding, that is, the energy needed to process ingested food.

Non-REE is an activity-related component including exercise and non-exercise activity thermogenesis. AT refers to changes in REE and non-REE, which are independent from changes in FFM and its composition.

Individuals with normal weight maintain their energy balance over a period of time in a remarkably accurate way. For example, a healthy adult weighing 75 kg typically consumes 3, kcal every day i. One study demonstrated that recording food intake for 2 weeks revealed interesting findings; compensatory intake occurred with a lag time of 3 to 4 days when more than the average energy intake was consumed.

It is also possible to examine the trend of food intake over a long period of time. The Food and Agriculture Organization of the United Nations calculated that the average American consumes more than 3, kcal a day, or a total of 1.

Department of Agriculture calculates that a sedentary adult male requires 2, kcal a day, or , kcal a year, and those who are physically active require 2, kcal a day, an annual intake of 1.

Without the intervention of compensatory mechanisms, this significant excess of energy intake over expenditure would result in a massive increase in body weight every year. Therefore, the mismatch in energy balance on a day-to-day basis is corrected by the energy homeostasis system over long periods of time.

Two models have dominated the discussion regarding the mechanisms by which body weight is regulated between energy intake and expenditure. The set point model suggests that there is an active feedback mechanism linking adipose tissue stored energy to food intake and expenditure via a set point, presumably encoded in the brain.

The biological mechanisms that control energy balance are programmed by environmental factors, and the point at which body weight is maintained may change. In this system, the level of the energy reservoir fat stores settles to an equilibrium that is determined by inflow food intake , which is matched to outflow energy expenditure , as the rate of outflow is passively related to the level of the reservoir.

Hence, the settling point model explains the increasing prevalence of obesity as a result of food availability, more exposure to food signals i. There is no doubt that changes in the availability of food and its increased caloric content have played a major role in the obesity epidemic.

However, public health advice to reduce food intake has not provided a fundamental solution in resolving obesity. Although high calorie intake was an important cause of the problem initially, its reduction is not able to solve it.

Reducing calorie intake results in a decrease in body weight, followed by strong physiological adaptations to regain weight. According to dynamic energy balance, weight loss results from a negative energy balance and changes in body composition Fig. It is not continuous but ends in a curvilinear way when a new equilibrium between energy intake and energy expenditure is reached.

During caloric restriction, the first phase of weight loss is rapid and lasts from a few days to a month phase 1 ; this is followed by a second phase characterized by a slower weight loss phase 2.

AT is observed in lean as well as overweight subjects, independent of the weight loss strategy. During phase 1, more FFM decreases than fat mass. During the first week of caloric restriction, hepatic glycogen stores are depleted due to an immediate drop in insulin secretion, resulting in natriuresis and a reduction in extracellular water.

A negative nitrogen balance from protein loss results primarily from gastrointestinal tract and liver proteins involved with nutrient processing in the early phase of weight loss.

Later, proteolysis occurs in skeletal muscle and other visceral organs. Thus, water associated with protein catabolism is an important contributor to the rapid weight loss observed in phase 1. The combined effects of glycogen, protein, and fluid loss largely account for the rapid weight loss of phase 1 compared with the slower rates observed in phase 2.

Results indicate that regulation of AT occurred mainly during phase 1 because the AT became manifest within the first 3 days after caloric restriction, with no further changes during phase 2. After a decrease in body weight, the AT decreased with leptin reduction due to body fat depletion.

TEE also remained lower due to reduced AT in the non-REE; it was accompanied by increased skeletal muscle work efficiency and decreased plasma levels of leptin and T3 associated with low sympathetic nervous system activity. It is possible to obtain important information about changes in body composition and energy expenditure after dramatic weight loss from the results of an American competition reality show.

After that, it was recommended that they continue eating and exercise interventions at the same level back at home. At week 30, all participants were tested for body composition and energy expenditure, i. On average, participants lost more than one-third of their initial body weight initial mean BMI, Participants who rapidly lost a significant amount of weight through diet restriction and vigorous physical activity preserved much of their FFM.

Relative preservation of FFM was likely due to maintenance or possible increase of skeletal muscle tissue during vigorous exercise. A substantial decrease in resting metabolism during active weight loss might not be avoided by the addition of an exercise program. Suppression of resting metabolism continued after 6 years of competition, despite substantial weight regains.

On the other hand, the magnitude of metabolic adaptation increased 6 years after the competition. Therefore, long-term weight loss requires vigilant combat against persistent metabolic adaptation that acts to proportionally counter ongoing efforts to reduce body weight.

Analysis using the computational model of metabolism by Hall et al. Metabolic adaptation occurs in energy expenditure even when individuals attempt to lose weight by exercise alone without diet control. Thus, both energy expenditure and energy intake were affected by adaptive metabolic response to weight loss due to exercise.

Thus, weight loss, whether diet-induced or exercise-driven, leads to decrease in TEE, REE, and non-REE. Mechanisms associated with reduction of TEE following weight loss are likely to be related to decreased body mass and enhanced metabolic efficiency.

Using a mathematical model that reflects dynamic energy balance, it is possible to make personalized calorie and physical activity plans to reach a goal weight within a specific time period and to maintain it afterward. By modifying the initial conditions of the model to represent an individual person, the simulator can be used for personalized goal setting and behavioral intervention planning.

In reality, however, outpatient weight-loss interventions typically result in maximum weight loss after 6 to 8 months, followed by gradual weight regain over subsequent years. A common explanation for the weight loss plateau at 6 to 8 months is that energy expenditure decreases to match energy intake, pausing further weight loss metabolic compensation.

Weight regain occurs as individuals gradually weaken compliance with the diet that has resulted in weight loss behavioral compensation. Hall et al. Energy intake gradually increased and returned to the original weight-maintenance level in the first year and was maintained there for the remaining 3-year simulation.

The simulated TEE showed that negative energy balance was achieved for less than 8 months, after which positive energy balance and weight regain occurred. This predicted pattern of energy intake means that weight loss continues for several months at the same time that average energy intake slowly increases.

The dieter may then misconstrue that maintenance of lifestyle change is not essential for continuing weight loss when weight regain has already begun.

Even if the original lifestyle is resumed within the first year, the weight gain will gradually recur over many years because weight change occurs slowly.

As mentioned earlier, energy intake and expenditure are tightly coupled over prolonged time intervals in adults living independently. This is equivalent to an average increase of energy stored in body fat and lean tissue divided by the time needed to store the energy.

As these changes have persisted for the last three decades, the obesity epidemic has become a global problem. The maintenance energy gap estimates the increased energy intake needed to maintain higher average weights following the obesity epidemic.

Table 1 shows data from the — Korea National Health and Nutrition Examination Surveys KNHANES. Swinburn et al. Applying this result to the KNHANES data, the energy maintenance gap of kcal since would be predicted to result in a weight gain of 4. In reality, the average weight gain of men was only 2.

This is a substantial change and shows that the reversal of obesity would require substantially large changes in terms of energy balance. My podcast changed me Can 'biological race' explain disparities in health?

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Medical News Today. Health Conditions Health Products Discover Tools Connect. Ways to lose subcutaneous fat. Medically reviewed by Daniel Bubnis, M. Causes Difficulty to lose Strategies to shed Connection to health Subcutaneous fat is fat that is visible just under the skin.

What causes it and why is it hard to lose? Why is it so hard to lose? Strategies for shedding subcutaneous fat. Subcutaneous fat and health. How we reviewed this article: Sources. Medical News Today has strict sourcing guidelines and draws only from peer-reviewed studies, academic research institutions, and medical journals and associations.

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Related Coverage. Low-fat vs. low-carb: Which diet is best for weight loss?

Ways to lose subcutaneous fat Endocr Rev ; Ways of reducing it include swapping some carbohydrates for protein, doing aerobic exercise, and managing mental health issues. It is also possible to examine the trend of food intake over a long period of time. Physical activity facts and statistics. Thus, in an attempt to generate an animal model of obesity that more closely resembles this disease in humans, fat-enriched diets or high-fat HF diets have been extensively used to induce obesity in rodents [ 6 , 8 ].
Body Composition

This feedback loop may be part of an antioxidant defense mechanism that adapts prolonged mitochondrial superoxide production Scandroglio et al. Acetyl-CoA diversion may slow delivery of electron carriers such as NADH to the respiratory chain, thereby decreasing ROS production Armstrong et al.

Oxidative stress also impacts pyruvate dehydrogenase kinase 2 PDK2 inhibition of the pyruvate dehydrogenase complex PDC Hurd et al.

ROS oxidize critical cysteine residues, disabling PDK2, and supporting acetyl-CoA synthesis from glucose-derived pyruvate. Therefore, elevated mitochondrial superoxide and H 2 O 2 couples PDC activity with aconitase interruption to divert citrate from the TCA cycle to the cytoplasm as triglycerides during overnutrition.

These studies suggest persistent nutrient stress impairs the physiological behavior of crucial metabolic enzymes needed for balanced ATP generation and consumption. A variety of peroxidases, including catalase, glutathione peroxidases, and peroxiredoxins Prdxs that control the levels of H 2 O 2 in the cell and protect against ROS-induced damage by catalyzing the reduction of H 2 O 2 into water.

Along these lines, overexpression of catalase Anderson et al. The mitochondrial antioxidant peroxiredoxin 3 Prdx3 responds to oxidative stress and scavenges H 2 O 2.

Levels of Prdx3 are decreased in obese humans and mice, potentially contributing to oxidative stress intolerance Huh et al. Whole-body deletion of Prdx3 in mice causes obesity and increased expression of lipogenic genes in adipocytes, while decreasing expression of lipolytic genes.

As a result, hypertrophic adipocytes exclusively accumulate excess lipids and cannot enable appropriate energy balance control. In addition to altering the balance of lipogenesis and lipolysis, Prdx3-deficient adipocytes exhibited increased superoxide production, decreased mitochondrial potential, and altered adipokine expression, including decreased adiponectin.

Okuno et al. AKO mice leverage adipocyte-specific ablation of glutamate-cysteine ligase Gclc to disable the rate-limiting step in glutathione synthesis and increase ROS generation.

Insulin sensitivity was also reduced. Conversely, mice expressing rat catalase and human SOD1 under the aP2 promoter had the opposite phenotype.

These mice aP2-dTg showed reduced H 2 O 2 in subcutaneous and gonadal WAT. While these data argue that increasing mitochondrial antioxidants protects against oxidative stress in WAT, genetic alteration of other mitochondrial antioxidants reveal different phenotypes.

Manganese superoxide dismutase MnSOD is an important mitochondrial antioxidant that detoxifies superoxides Holley et al. Adipocyte-specific knockout of MnSOD protected against diet-induced WAT expansion and weight gain Han et al.

Mechanistically, MnSOD knockout in adipocytes triggered an adaptive stress response that activated mitochondrial biogenesis and enhanced mitochondrial fatty acid oxidation, thereby preventing diet-induced obesity and insulin resistance. Increased ROS levels correlated with Uncoupling Protein 1 UCP1 activation in subcutaneous WAT and higher energy expenditure Han et al.

These disparate features of mice that lack the Prdx3 and MnSOD genes coupled with therapeutic shortcomings of antioxidant therapies in human clinical trials Fusco et al.

The homeostatic systems that regulate oxidative stress in the lean state are largely repressed in obesity due to the accumulation of oxidized biomolecules within WAT. Excessive ROS irreversibly damages DNA, lipids, and proteins with adverse effects on cellular functions.

Increased oxidative stress can alter proteins and lipids through direct and indirect pathways that culminate in oxidation of side chains and lipid-protein adduction Grimsrud et al. Reactive oxygen species oxidation of lipids ultimately generates lipid aldehydes that modify DNA, proteins, RNA, and other lipid species Esterbauer et al.

Increased markers of lipid peroxidation, including thiobarbituric acid reactive substances TBARS and 8-epi-prostaglandin-F2α 8-epi-PGF2α are observed in individuals with higher BMI and waist circumference Furukawa et al.

Oxidized lipids and proteins preferentially accumulate in visceral depots compared to subcutaneous depots of obese mice Long et al. Lipid aldehydes are highly electrophilic and prone to irreversible nucleophilic attack by the side chains of lysine Lys , histidine His , and cysteine Cys residues of proteins, resulting in a covalent lipid-protein adduct termed protein carbonylation Schaur, ; Curtis et al.

Furthermore, Lys, His, and Cys residues often cluster within active sites of enzymes or critical structural motifs, so their stable modification by lipids generally leads to inhibition or deactivation of protein function.

However, recent work challenges the notion that ROS-driven modifications broadly degrade fat cell function.

Brown adipose tissue BAT contains elevated levels of mitochondrial superoxide, mitochondrial H 2 O 2 , and oxidized lipids that correlate with acute activation of thermogenesis Chouchani et al.

Mitochondrial ROS in BAT can converge on UCP1 C inducing cysteine sulfenylation -SOH Chouchani et al. Interestingly, UCP1 CA does not disable thermogenic responses in brown adipocytes but desensitizes the protein to adrenergic activation of uncoupled respiration.

Further exploration of physiological ROS signaling outputs and modifications may show how redox status in adipocytes contributes to energy balance.

Polyunsaturated fatty acids PUFAs are abundant in WAT and particularly sensitive to lipid peroxidation. One major consequence of lipid peroxidation is mitochondrial membrane damage Kowaltowski and Vercesi, Also, peroxidation of PUFAs results in the release of diffusible reactive lipid aldehydes.

Among the wide variety of reactive lipids formed through this mechanism, 4-hydroxy-non-enal 4-HNE derived from oxidation of n6 fatty acids and 4-hydroxy-hexenal 4-HHE from n3 fatty acid oxidation are the most widely studied in the context of adipose biology. The WAT of obese mice showed decreased metabolism of 4-HNE, while stress response proteins, including glutathione-S-transferase M1, glutathione peroxidase 1, and Prdx Grimsrud et al.

Lipid peroxidation end products can also inhibit insulin signaling as 4-HNE de-stabilizes IRS adapter proteins and insulin receptor β Demozay et al. Lipid peroxidation products also damage the function of transcription factors that contain zinc-finger motifs, histones, and other nuclear proteins of visceral fat cells isolated from obese mice Hauck et al.

The lipid peroxidation of transcriptional regulatory proteins presents a consolidated mechanism for retrograde ROS signaling from mitochondria to the nucleus. Although mitochondria are the most significant source of ROS, the discovery of lipid-protein adducts in the nucleus of adipocytes suggests either a different pool of ROS contributes to lipid peroxidation or a mechanism exists to sequester and shuttle reactive aldehydes to specific subcellular localizations Hauck et al.

As with ROS, the timing of protein carbonylation may be important for beneficial or pathologic effects. Acute carbonylation of substrates after exercise are potentially beneficial, while chronic accumulation of carbonylated proteins in the muscle and WAT of obese and sedentary individuals may be pathological and contribute to comorbidities of obesity Frohnert and Bernlohr, Additionally, ROS seem to be important in the cellular aspects of adipocyte differentiation.

Numerous studies demonstrate that mitochondrial biogenesis increases during adipocyte differentiation Wilson-Fritch et al. Dramatic expansion of mitochondrial content enables higher metabolic rates to overcome the energetic demands of differentiation. Induction of differentiation correlates with superoxide generation from complex III, conversion of superoxide to H 2 O 2 , and activation of transcriptional machinery necessary for adipogenesis Tormos et al.

et al. However, obesity-mediated ROS induction also restricts mitochondrial biogenesis and adipocyte differentiation. Higher accumulation of 4-HNE adducts occurs in cultured differentiating preadipocytes from insulin-resistant compared to insulin-sensitive individuals.

In this manner, treatment of primary subcutaneous preadipocytes from obese individuals with pathological levels of 4-HNE decreased markers associated with insulin sensitivity and mature fat cells Dasuri et al. Other studies demonstrate that treatment with antioxidants decreases differentiation Tormos et al.

Divergent in vitro and in vivo findings illustrate existing challenges in defining the specifics of ROS signaling and its connectivity to metabolic diseases.

Nutrient overload has been linked to the development of insulin resistance. One carbonylated protein of importance was GLUT4, whose carbonylation likely impairs insulin-stimulated glucose uptake.

Of note, systemic oxidative stress and insulin resistance did not coincide with inflammatory cytokines in plasma nor ER stress in WAT. These findings provide a causal link between oxidative stress and insulin resistance in humans. Mitochondrial metabolism is often altered in inherited diseases, such as inborn errors of metabolism IEMs that impinge upon ROS generation.

Inhibition of OXPHOS increases ROS generation due to a backlog of electrons in the various complexes, resulting in electron leak, ROS generation, and production of H 2 O 2.

In IEMs affecting the ETC or other pathways of ATP generation, increased oxidative stress is often observed, while the exact mechanisms for increased ROS production are unknown. It is hypothesized that mutations affecting the formation of the protein complexes in the ETC or mutations that modify their assembly increase ROS generation by facilitating electron leak Olsen et al.

Additionally, accumulation of toxic intermediates, often observed in IEMs, can increase the ROS generation by further decreasing OXPHOS activity, as in the case of medium-chain acyl-CoA dehydrogenase MCAD deficiency. MCAD deficiency reflects the accumulation of medium-chain fatty acid derivatives, including cisdecenoic acid, octanoate, and decanoate, with these metabolites altering levels of antioxidants and increasing markers of oxidative stress Schuck et al.

Intriguingly, IEMs display metabolic reprograming with a switch to glycolysis for both ATP production and muted ROS generation Olsen et al. Specifically, in myoclonic epilepsy with ragged red fibers MERRF , increased intracellular H 2 O 2 levels correspond with increased AMPK phosphorylation and expression of GLUT1, hexokinase II, and lactate dehydrogenase.

These results, as well as increased lactic acid production, all point to increased glycolysis De la Mata et al. In multiple acyl-CoA dehydrogenase deficiency MADD , mutations in ETFa , ETFb , or ETFDH , lead to decreased ATP production with an accumulation of organic acids, including glutaric acid as well as acyl-carnitines.

A subset of these patients is riboflavin responsive RR-MADD with high dose riboflavin alleviating some symptoms. Similar to MERRF, many RR-MADD patients exhibit increased oxidative stress Cornelius et al. This defect may be due to defective electron transfer and increased electron leak from the misfolded ETFDH protein and decreased binding of CoQ10 Cornelius et al.

Treatment with CoQ10, but not riboflavin, decreased ROS levels Cornelius et al. Analysis of mitochondrial function from RR-MADD fibroblasts showed increased mitochondrial fragmentation and reduced β-oxidation, while supplementation with the antioxidant CoQ10 decreased fragmentation and mitophagy Cornelius et al.

While obesity and IEMs are distinct disorders, both conditions impinge on energy balance in WAT. Even though these disorders have very different manifestations, oxidative stress plays an important role in both and may be a therapeutic target.

For example, CoQ10 is often given as a broad-spectrum treatment to individuals with IEMs, and while its effectiveness is debated, the anti-inflammatory effects may be beneficial in reducing oxidative stress and the pathogenesis of the disease Cornelius et al. Mitochondria represent control centers of many metabolic pathways.

Interventions that enhance adipocyte mitochondrial function may also improve whole-body insulin sensitivity. Mitigation of mitochondrial ROS production and oxidative stress may be a possible therapeutic target in type 2 diabetes and IEMs because some mitochondrial-targeted antioxidants and other small molecule drugs improve metabolic profiles in mouse models Feillet-Coudray et al.

Thiazolidinediones TZDs are PPARγ agonists used for treating type 2 diabetes Kelly et al. TZDs, such as rosiglitazone and pioglitazone, enhance insulin sensitivity by improving adipokine profiles Maeda et al. TZDs also promote insulin sensitivity by directing fatty acids to subcutaneous fat, rather than visceral fat.

Subcutaneous fat expandability, even in the context of obesity and type 2 diabetes, correlates with insulin sensitivity in rodents and humans Ross et al. Numerous in vitro and in vivo studies demonstrate TZDs enhance mitochondrial biogenesis, content, function, and morphology.

Rosiglitazone also induces cellular antioxidant enzymes responsible for the removal of ROS generated by increased mitochondrial activity in adipose tissue of diabetic rodents Rong et al.

Taken together, TZDs impact WAT mitochondrial function in multiple ways that ultimately improve systemic fat metabolism and insulin sensitivity. Other therapeutic strategies include mitochondria-targeted scavengers Smith et al. However, these methods to enhance mitochondrial function display a narrow therapeutic range that limits safe use for obesity.

Although the development of insulin resistance does not require impaired mitochondrial function Hancock et al. Aerobic exercise and caloric restriction disrupt this vicious loop, potentially by preventing accumulation of injured mitochondrial proteins with substantial improvement of insulin sensitivity.

In insulin-resistant people, aerobic exercise stimulates both mitochondrial biogenesis and efficiency concurrent with an enhancement of insulin action Mul et al. Ultimately, exercise engages pathways that reduce ROS coupled with insulin sensitivity and improved mitochondrial function in WAT.

Obesity is the result of excessive expansion of WAT depots due to a chronic imbalance between energy intake and expenditure. Many studies demonstrate that oxidative stress in fat cells links obesity and its comorbidities.

The fact that WAT remains the sole organ for storing surfeit lipid renders the macromolecules in adipocytes particularly vulnerable to carbonylation and other modifications driven by oxidative stress.

Prolonged oxidative stress negatively influences endocrine and homeostatic performance of WAT, including disruption of hormone secretion, elevation of serum lipids, inadequate cellular antioxidant defenses, and impaired mitochondrial function Figure 2.

Metabolic challenges, such as persistent nutrient intake and sedentary behaviors that promote impaired glucose and lipid handling, also elevate mitochondrial ROS production to cause adipocyte dysfunction.

Consequently, adipocytes cannot engage appropriate transcriptional and energetic responses to enable insulin sensitivity. Figure 2. Impact of oxidative stress on adipocyte function. Increased plasma glucose and free fatty acids contribute to increased oxidative stress by increasing the production of reactive oxygen species ROS and decreasing antioxidant concentrations.

Increased oxidative stress occurs via enzymes in the cytoplasm, such as NADPH oxidase, and the mitochondria. The oxidative environment increases lipid storage resulting in hypertrophic adipocytes.

Additionally, increased mitochondrial ROS mtROS alters the activity state of metabolic enzymes either directly or by changing the oxidative state of protein side-chains or by other post-translational modifications, including lipid peroxidation and protein carbonylation.

Cumulatively, increased adipocyte oxidative stress decreases adipogenesis and secretion of adipokines, leading to unbalanced energy homeostasis, insulin resistance, and type 2 diabetes.

The increasing prevalence of obesity suggests lifestyle intervention as the principal method to treat obesity is unlikely to succeed. Currently, all available anti-obesity medications act by limiting energy intake through appetite suppression or inhibition of intestinal lipid absorption.

However, these medications are largely ineffective and often have adverse side effects. The central role of mitochondria in nutrient handling provides a logical entry point for improving metabolism in obesity. While approaches to understanding and intervening in oxidative damage evolve, exploration of mitochondria redox balance may enable development of dietary and small molecule therapies for obesity and its comorbidities.

This work was funded by the American Diabetes Association IBS and NIH R01DK The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Acosta, M. Coenzyme Q biosynthesis in health and disease. Acta , — doi: PubMed Abstract CrossRef Full Text Google Scholar. Ahmed, M. Proteomic analysis of human adipose tissue after rosiglitazone treatment shows coordinated changes to promote glucose uptake.

Obesity 18, 27— Akl, M. Perturbed adipose tissue hydrogen peroxide metabolism in centrally obese men: association with insulin resistance. PLoS One e Anderson, E. Mitochondrial H2O2 emission and cellular redox state link excess fat intake to insulin resistance in both rodents and humans.

Armstrong, J. The redox regulation of intermediary metabolism by a superoxide-aconitase rheostat. Bioessays 26, — Barbosa, M. Hydrogen peroxide production regulates the mitochondrial function in insulin resistant muscle cells: effect of catalase overexpression. Bjelakovic, G.

Antioxidant supplements to prevent mortality. JAMA , — Antioxidant supplements and mortality. Care 17, 40— Boden, G. Excessive caloric intake acutely causes oxidative stress, GLUT4 carbonylation, and insulin resistance in healthy men.

Boden, M. Overexpression of manganese superoxide dismutase ameliorates high-fat diet-induced insulin resistance in rat skeletal muscle. Bogacka, I. Structural and functional consequences of mitochondrial biogenesis in human adipocytes in vitro. Bournat, J. Mitochondrial dysfunction in obesity.

Diabetes Obes. Boyle, P. Effects of pioglitazone and rosiglitazone on blood lipid levels and glycemic control in patients with type 2 diabetes mellitus: a retrospective review of randomly selected medical records.

Chappuis, B. Differential effect of pioglitazone PGZ and rosiglitazone RGZ on postprandial glucose and lipid metabolism in patients with type 2 diabetes mellitus: a prospective, randomized crossover study. Diabetes Metab. Chouchani, E. Mitochondrial ROS regulate thermogenic energy expenditure and sulfenylation of UCP1.

Nature , — Mitochondrial reactive oxygen species and adipose tissue thermogenesis: bridging physiology and mechanisms. Cornelius, N. Secondary coenzyme Q10 deficiency and oxidative stress in cultured fibroblasts from patients with riboflavin responsive multiple Acyl-CoA dehydrogenation deficiency.

Cellular consequences of oxidative stress in riboflavin responsive multiple acyl-CoA dehydrogenation deficiency patient fibroblasts. Curtis, J. Protein carbonylation and metabolic control systems.

Trends Endocrinol. Dasuri, K. Role of physiological levels of 4-hydroxynonenal on adipocyte biology: implications for obesity and metabolic syndrome. Free Radic. Davies, M. Protein oxidation and peroxidation.

De la Mata, M. Recovery of MERRF fibroblasts and cybrids pathophysiology by coenzyme Q Neurotherapeutics 9, — Deeg, M. Pioglitazone and rosiglitazone have different effects on serum lipoprotein particle concentrations and sizes in patients with type 2 diabetes and dyslipidemia.

Diabetes Care 30, — Demozay, D. FALDH reverses the deleterious action of oxidative stress induced by lipid peroxidation product 4-hydroxynonenal on insulin signaling in 3T3-L1 adipocytes.

Elrayess, M. Escribano-Lopez, I. The mitochondrial antioxidant SS increases SIRT1 levels and ameliorates inflammation, oxidative stress and leukocyte-endothelium interactions in type 2 diabetes. Esterbauer, H. Chemistry and biochemistry of 4-hydroxynonenal, malonaldehyde and related aldehydes.

Fazakerley, D. Mitochondrial oxidative stress causes insulin resistance without disrupting oxidative phosphorylation. Feillet-Coudray, C. The mitochondrial-targeted antioxidant MitoQ ameliorates metabolic syndrome features in obesogenic diet-fed rats better than Apocynin or Allopurinol.

Fouret, G. The mitochondrial-targeted antioxidant, MitoQ, increases liver mitochondrial cardiolipin content in obesogenic diet-fed rats. Frohnert, B. Protein carbonylation, mitochondrial dysfunction, and insulin resistance. Increased adipose protein carbonylation in human obesity.

Positive self-talk can help manage thoughts and emotions. Many of these products are not evaluated by the Food and Drug Administration for efficacy, and may contain hidden ingredients or make false claims.

You can use this Supplement Safety Scorecard in order to screen your supplement for safety. You do not have to lose a lot of weight in order to see health benefits.

People who lose weight gradually ~. As stated by Flynn et al. To successfully lose 2 pounds per week, that reduction would have to be doubled to 1, calories per day. Attempting to lose 2 pounds or more per week would require a calorie reduction too drastic to be maintained and too restrictive to be healthy.

Thus, the recommendation of combining diet and exercise is the most effective method for experiencing weight loss.

Subtracting calories of food intake and exerting calories in exercise will provide that same calorie reduction, but in a manner that is far easier to maintain, and certainly more enjoyable. Centers for Disease Control and Prevention. Medical complications of obesity. The new Ab normal.

Healthy weight. Losing weight. The health effects of overweight and obesity. How much physical activity do adults need? Getting started with physical activity for a healthy w eight? Comana, F. Resting metabolic rate: How to calculate and improve yours.

Derma, F. RMR calculator — Resting metabolic rate. Omni Calculator. Evans, M. Flynn, S. Concepts of fitness and wellness 2 nd ed.

Nursing and Health Sciences Open Textbooks. Frey, M. Signs that you are underweight. Hefele, L. Brain Bites — Energy Balance.

Kravitz, L. Getting a grip on body composition. Lee Health. BMI vs Body Fat. MD Anderson Cancer Center. How to measure your waist circumference. Office of Disease Prevention and Health Promotion. Activity planner. Operation Supplement Safety. Screen your supplement for safety.

Sarwer, D.

Background

In IEMs affecting the ETC or other pathways of ATP generation, increased oxidative stress is often observed, while the exact mechanisms for increased ROS production are unknown.

It is hypothesized that mutations affecting the formation of the protein complexes in the ETC or mutations that modify their assembly increase ROS generation by facilitating electron leak Olsen et al.

Additionally, accumulation of toxic intermediates, often observed in IEMs, can increase the ROS generation by further decreasing OXPHOS activity, as in the case of medium-chain acyl-CoA dehydrogenase MCAD deficiency.

MCAD deficiency reflects the accumulation of medium-chain fatty acid derivatives, including cisdecenoic acid, octanoate, and decanoate, with these metabolites altering levels of antioxidants and increasing markers of oxidative stress Schuck et al. Intriguingly, IEMs display metabolic reprograming with a switch to glycolysis for both ATP production and muted ROS generation Olsen et al.

Specifically, in myoclonic epilepsy with ragged red fibers MERRF , increased intracellular H 2 O 2 levels correspond with increased AMPK phosphorylation and expression of GLUT1, hexokinase II, and lactate dehydrogenase.

These results, as well as increased lactic acid production, all point to increased glycolysis De la Mata et al. In multiple acyl-CoA dehydrogenase deficiency MADD , mutations in ETFa , ETFb , or ETFDH , lead to decreased ATP production with an accumulation of organic acids, including glutaric acid as well as acyl-carnitines.

A subset of these patients is riboflavin responsive RR-MADD with high dose riboflavin alleviating some symptoms. Similar to MERRF, many RR-MADD patients exhibit increased oxidative stress Cornelius et al.

This defect may be due to defective electron transfer and increased electron leak from the misfolded ETFDH protein and decreased binding of CoQ10 Cornelius et al. Treatment with CoQ10, but not riboflavin, decreased ROS levels Cornelius et al.

Analysis of mitochondrial function from RR-MADD fibroblasts showed increased mitochondrial fragmentation and reduced β-oxidation, while supplementation with the antioxidant CoQ10 decreased fragmentation and mitophagy Cornelius et al. While obesity and IEMs are distinct disorders, both conditions impinge on energy balance in WAT.

Even though these disorders have very different manifestations, oxidative stress plays an important role in both and may be a therapeutic target. For example, CoQ10 is often given as a broad-spectrum treatment to individuals with IEMs, and while its effectiveness is debated, the anti-inflammatory effects may be beneficial in reducing oxidative stress and the pathogenesis of the disease Cornelius et al.

Mitochondria represent control centers of many metabolic pathways. Interventions that enhance adipocyte mitochondrial function may also improve whole-body insulin sensitivity.

Mitigation of mitochondrial ROS production and oxidative stress may be a possible therapeutic target in type 2 diabetes and IEMs because some mitochondrial-targeted antioxidants and other small molecule drugs improve metabolic profiles in mouse models Feillet-Coudray et al. Thiazolidinediones TZDs are PPARγ agonists used for treating type 2 diabetes Kelly et al.

TZDs, such as rosiglitazone and pioglitazone, enhance insulin sensitivity by improving adipokine profiles Maeda et al. TZDs also promote insulin sensitivity by directing fatty acids to subcutaneous fat, rather than visceral fat. Subcutaneous fat expandability, even in the context of obesity and type 2 diabetes, correlates with insulin sensitivity in rodents and humans Ross et al.

Numerous in vitro and in vivo studies demonstrate TZDs enhance mitochondrial biogenesis, content, function, and morphology.

Rosiglitazone also induces cellular antioxidant enzymes responsible for the removal of ROS generated by increased mitochondrial activity in adipose tissue of diabetic rodents Rong et al. Taken together, TZDs impact WAT mitochondrial function in multiple ways that ultimately improve systemic fat metabolism and insulin sensitivity.

Other therapeutic strategies include mitochondria-targeted scavengers Smith et al. However, these methods to enhance mitochondrial function display a narrow therapeutic range that limits safe use for obesity.

Although the development of insulin resistance does not require impaired mitochondrial function Hancock et al. Aerobic exercise and caloric restriction disrupt this vicious loop, potentially by preventing accumulation of injured mitochondrial proteins with substantial improvement of insulin sensitivity.

In insulin-resistant people, aerobic exercise stimulates both mitochondrial biogenesis and efficiency concurrent with an enhancement of insulin action Mul et al.

Ultimately, exercise engages pathways that reduce ROS coupled with insulin sensitivity and improved mitochondrial function in WAT. Obesity is the result of excessive expansion of WAT depots due to a chronic imbalance between energy intake and expenditure.

Many studies demonstrate that oxidative stress in fat cells links obesity and its comorbidities. The fact that WAT remains the sole organ for storing surfeit lipid renders the macromolecules in adipocytes particularly vulnerable to carbonylation and other modifications driven by oxidative stress.

Prolonged oxidative stress negatively influences endocrine and homeostatic performance of WAT, including disruption of hormone secretion, elevation of serum lipids, inadequate cellular antioxidant defenses, and impaired mitochondrial function Figure 2. Metabolic challenges, such as persistent nutrient intake and sedentary behaviors that promote impaired glucose and lipid handling, also elevate mitochondrial ROS production to cause adipocyte dysfunction.

Consequently, adipocytes cannot engage appropriate transcriptional and energetic responses to enable insulin sensitivity. Figure 2. Impact of oxidative stress on adipocyte function. Increased plasma glucose and free fatty acids contribute to increased oxidative stress by increasing the production of reactive oxygen species ROS and decreasing antioxidant concentrations.

Increased oxidative stress occurs via enzymes in the cytoplasm, such as NADPH oxidase, and the mitochondria. The oxidative environment increases lipid storage resulting in hypertrophic adipocytes. Additionally, increased mitochondrial ROS mtROS alters the activity state of metabolic enzymes either directly or by changing the oxidative state of protein side-chains or by other post-translational modifications, including lipid peroxidation and protein carbonylation.

Cumulatively, increased adipocyte oxidative stress decreases adipogenesis and secretion of adipokines, leading to unbalanced energy homeostasis, insulin resistance, and type 2 diabetes. The increasing prevalence of obesity suggests lifestyle intervention as the principal method to treat obesity is unlikely to succeed.

Currently, all available anti-obesity medications act by limiting energy intake through appetite suppression or inhibition of intestinal lipid absorption. However, these medications are largely ineffective and often have adverse side effects. The central role of mitochondria in nutrient handling provides a logical entry point for improving metabolism in obesity.

While approaches to understanding and intervening in oxidative damage evolve, exploration of mitochondria redox balance may enable development of dietary and small molecule therapies for obesity and its comorbidities.

This work was funded by the American Diabetes Association IBS and NIH R01DK The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Acosta, M. Coenzyme Q biosynthesis in health and disease. Acta , — doi: PubMed Abstract CrossRef Full Text Google Scholar. Ahmed, M. Proteomic analysis of human adipose tissue after rosiglitazone treatment shows coordinated changes to promote glucose uptake.

Obesity 18, 27— Akl, M. Perturbed adipose tissue hydrogen peroxide metabolism in centrally obese men: association with insulin resistance. PLoS One e Anderson, E. Mitochondrial H2O2 emission and cellular redox state link excess fat intake to insulin resistance in both rodents and humans.

Armstrong, J. The redox regulation of intermediary metabolism by a superoxide-aconitase rheostat. Bioessays 26, — Barbosa, M. Hydrogen peroxide production regulates the mitochondrial function in insulin resistant muscle cells: effect of catalase overexpression.

Bjelakovic, G. Antioxidant supplements to prevent mortality. JAMA , — Antioxidant supplements and mortality. Care 17, 40— Boden, G.

Excessive caloric intake acutely causes oxidative stress, GLUT4 carbonylation, and insulin resistance in healthy men. Boden, M. Overexpression of manganese superoxide dismutase ameliorates high-fat diet-induced insulin resistance in rat skeletal muscle.

Bogacka, I. Structural and functional consequences of mitochondrial biogenesis in human adipocytes in vitro. Bournat, J.

Mitochondrial dysfunction in obesity. Diabetes Obes. Boyle, P. Effects of pioglitazone and rosiglitazone on blood lipid levels and glycemic control in patients with type 2 diabetes mellitus: a retrospective review of randomly selected medical records.

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Lushchak, O. Aconitase post-translational modification as a key in linkage between Krebs cycle, iron homeostasis, redox signaling, and metabolism of reactive oxygen species. Redox Rep. Maeda, N. PPARgamma ligands increase expression and plasma concentrations of adiponectin, an adipose-derived protein.

Miyazaki, Y. Effect of pioglitazone on abdominal fat distribution and insulin sensitivity in type 2 diabetic patients. In fact, the CDC estimates obesity now affects 1 in 5 adolescents and children in the United States. The CDC estimates the prevalence of adult obesity was Research indicates obesity is associated with a greater risk of various health concerns, including heart disease, diabetes, stroke, and cancer CDC, The image below indicates adult obesity prevalence by state and territory using self-reported information from the Behavioral Risk Factor Surveillance System BRFSS.

Body fat percent is often estimated using skinfolds, bioelectrical impedance analysis BIA , and hydrostatic weighing. Body Mass Index BMI is another calculation used to assess body composition.

It is important to note, there are some limitations with calculating BMI. BMI accuracy as an indicator of body fat appears to be higher in individuals with higher levels of BMI and body fat Bray et al. At the same BMI, older adults generally tend to have greater body fat compared with younger adults CDC, Furthermore, athletes may have a higher BMI due to increased muscle mass rather than increased body fat CDC, Waist Circumference helps assess body fat distribution.

Excess abdominal fat can increase the risk of diabetes, heart disease, and stroke CDC, In order to measure your waist correctly, stand and place a measuring tape around your mid-section just above your hipbones.

You should measure your waist after breathing out. Women with a circumference over 35 inches and men with a circumference over 40 inches are at higher health risk CDC, Overweight and obesity are associated with an increased risk for multiple health concerns and diseases:.

It is important to note the health effects associated with being underweight as well. With this concept in mind, it is important to focus on maintaining a healthy body weight.

Tracking your diet and physical activity can be a great step in managing weight. The CDC provides tracking tools you can use: Food Diary and Physical Activity Diary.

Aim for at least 3 entries each day and try to stay consistent in your tracking. You can use this interactive body weight planner in order to calculate the number of calories and physical activity required in order to reach your goal weight and maintain it: Body Weight Planner.

Move Your Way Physical Activity Plan. Focus on setting SMART goals. Small lifestyle changes can add up to big improvements in health. Any physical activity is better than none. Monitor your internal thoughts and recognize how negative emotions can impede your progress.

Positive self-talk can help manage thoughts and emotions. Many of these products are not evaluated by the Food and Drug Administration for efficacy, and may contain hidden ingredients or make false claims.

You can use this Supplement Safety Scorecard in order to screen your supplement for safety. You do not have to lose a lot of weight in order to see health benefits. People who lose weight gradually ~. As stated by Flynn et al. To successfully lose 2 pounds per week, that reduction would have to be doubled to 1, calories per day.

Attempting to lose 2 pounds or more per week would require a calorie reduction too drastic to be maintained and too restrictive to be healthy. Thus, the recommendation of combining diet and exercise is the most effective method for experiencing weight loss. Subtracting calories of food intake and exerting calories in exercise will provide that same calorie reduction, but in a manner that is far easier to maintain, and certainly more enjoyable.

Centers for Disease Control and Prevention. Medical complications of obesity. The new Ab normal. Healthy weight. Losing weight.

Subcutaneous fat is BMI Measurement that is visible Subcutaheous under the skin. Ways of Hydrating cleansing formulas Muscle-preserving Fat Burner include Subcutaneoua some carbohydrates for ablance, doing aerobic Hydrating cleansing formulas, and managing mental health issues. Subcutaneous fat is normally harmless and may even protect against some diseases. Visceral fat is fat that surrounds the organs. Though it is not visible from the outside, it is associated with numerous diseases. It is possible to lose both subcutaneous and visceral fat.

Author: Bagami

5 thoughts on “Subcutaneous fat and energy balance

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