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Glucose metabolism pathways disorders

Glucose metabolism pathways disorders

Article PubMed PubMed Mtabolism Google Scholar Hanagasi, H. ATP-citrate lyase controls a glucose-to-acetate metabolic switch. Google Scholar Lafontan, M. Glucose metabolism pathways disorders

Glucose metabolism pathways disorders -

What are the myths and facts of metabolism? Can you speed…. An endocrinologist specializes in hormone-related health conditions ranging from thyroid problems to diabetes and insomnia.

Here, learn why people see…. Diabetes is a metabolic disorder that affects how the body processes energy from food. Learn more about diabetes and metabolism here. Phenylketonuria is a rare genetic condition that affects how amino acids are broken down in the body.

Learn more about how the condition is managed. Gaucher's disease is a inherited disease that results in a build up of lipids.

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Medical News Today. Health Conditions Health Products Discover Tools Connect. What to know about metabolic disorders. Medically reviewed by Avi Varma, MD, MPH, AAHIVS, FAAFP — By Aaron Kandola — Updated on June 26, Definition Causes Common disorders Common symptoms Diagnosis Treatment options When to see a doctor Summary Metabolic disorders are conditions that affect any aspect of metabolism.

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Atlantic diet may help prevent metabolic syndrome. However, the exact mechanism of how PKM2 regulates LRP-1 is unclear and will remain an area for future research. In addition, nuclear PKM2 can activate STAT3 and drive the transcription of pro-inflammatory genes IL-6 and IL-1β in a pSTAT3-dependent manner, exacerbating the inflammatory response [ ].

The above findings suggest that the glucose-ROS-PKM2-STAT3 axis and the search for PKM2 inhibitors are new directions for anti-inflammatory interventions in cardiovascular disease. Lactate dehydrogenase LD or LDH is a tetrameric enzyme that catalyzes the redox reaction between pyruvate and L-lactate and is one of the key enzymes of glycolysis.

In mammals, LDH has three subunits, LDHA, LDHB, and LDHC, which can constitute six tetrameric isoenzymes. Of these, LDHA is found mainly in skeletal muscle and liver, and is also known as the M subunit; LDHB is found mainly in the myocardium, brain, kidney, and erythrocytes [ ].

LDHA and LDHB can form homo- or heterotetramers LDH LDH1, LDH2, LDH3, LDH4, and LDH5 , which are expressed predominantly in the cytoplasm [ ]. Different isoenzymes have different catalytic roles.

LDHA catalyzes the conversion of pyruvate to lactate, while LDHB catalyzes the conversion of lactate to pyruvate [ ]. LDH6 is composed of homologous LDHC LDH-C4 , which is found primarily in human testes and spermatozoa and is associated with male fertility [ ]. Control of metabolic conversion is an important factor in cardiac repair after myocardial infarction and can effectively mitigate the loss of regenerative capacity in the mammalian heart [ ].

One study found that overexpression of LDHA induced metabolic reprogramming, stimulating CM proliferation by alleviating ROS and inducing M2 macrophage polarization [ ], facilitating cardiac remodeling, suggesting that LDHA may be an effective target to promote cardiac repair after myocardial infarction [ ].

Cardiac hypertrophy is an enlargement of the myocardium due to overload stress and is a major cause of heart failure [ ]. Metabolic remodeling is an early event in this process [ 57 , ]. Cardiac pressure overload can significantly upregulate LDHA expression in the heart, and LDHA deficiency in cardiomyocytes can lead to defective cardiac hypertrophy and heart failure.

In contrast, lactate can stimulate ERK extracellular signal-regulated kinase expression by stabilizing NDRG3 N-myc downstream-regulated gene 3 to rescue growth defects caused by LDHA knockdown [ ]. Furthermore, LDHB plays an important role in the treatment of Ang II-induced cardiomyocyte hypertrophy.

A miRp inhibitor has been found to inhibit Ang II-induced cardiomyocyte hypertrophy by promoting LDHB expression [ ]. Yamaguchi et al. found that serum LDH may also be an important predictor of , and day all-cause mortality in patients with acute decompensated heart failure, suggesting that serum LDH has important prognostic value in acute decompensated heart failure [ ].

Aortic dissection AD is a disease with a high mortality rate and a lack of effective drug therapy. Recent studies have suggested that AD progression may be closely linked to glucose metabolism.

At the same time, the upregulation of lactate, a product of LDHA, was also able to stabilize and promote the growth and phenotypic transformation of cardiomyocytes and VSMC [ ]. Therefore, we hypothesized that LDHA and its product lactate may be therapeutic targets for AD Fig.

In the failing heart, PKM2 tetramers bind directly to p53 and inhibit p53 transcriptional activity and apoptosis in the high oxidative state, thereby alleviating the progression of heart failure. However, they are enhanced in the low-oxidized state, and the small molecules TEPP and 2-DG can promote PKM2 tetramer formation.

When RIP3 translocates to mitochondria, it induces elevated PGAM5S expression, promotes Ser dephosphorylation on Drp-1, and facilitates mitochondrial fission. Pkm2 directly interacts with β-linker protein Ctnnb1 in the cytoplasm of cardiomyocytes CM , preventing translocation of Ctnnb1 to the nucleus, and subsequently repressing proliferation-related target genes, such as Myc and Cyclin D1.

When Pkm2 translocates to the nucleus, it can directly interact with Ctnnb1 in the nucleus of cardiomyocytes to form a complex that cooperates with T-cell factor 4 TCF4 , up-regulates its downstream targets Cy-clin-D1 and C-Myc, and transcriptionally induces genes encoding anti-apoptotic proteins.

The polyol pathway is the process of oxidative reduction of glucose to fructose, which involves two key enzymes, aldose reductase AR and sorbitol dehydrogenase SDH. Of these, AR reduces glucose to sorbitol while its cofactor, NADPH, is oxidized to NADP. SDH oxidizes sorbitol to fructose while reducing NAD to NADH [ 12 , ].

This pathway is thought to be strongly implicated in diabetic and nondiabetic myocardial ischemic injury, primarily by causing cellular oxidative stress and late AGEs end products of glycosylation formation to exacerbate ischemic myocardial injury [ , ].

In addition, the clearance of ROS requires the involvement of reduced glutathione GSH , a cofactor of glutathione reductase GR , and its depletion leads to a decrease in the level of reduced GSH, which prevents the clearance of ROS and exacerbates the oxidative stress injury [ ].

Second, overactivation of the polyol pathway accumulates excess NADH in the second step, which is a substrate for NADH oxidase and can lead to the production of more superoxide anions [ ]. Finally, fructose produced by the polyol pathway can be further metabolized into fructosephosphate and 3-deoxyglucosone, increasing the formation of AGEs [ ].

Therefore, the novel therapy of protection against ischemic cardiomyopathy through the inhibitory effect of polyol or aldose reductase pathways has attracted interest.

In addition, recent studies have found that elevated myocardial fructose and SDH may be associated with diabetic patients with diastolic dysfunction.

Fructose exacerbates the lipotoxicity of diabetic cardiomyopathy by promoting the formation of cytoplasmic lipid inclusion bodies in cardiomyocytes, and the inhibition of SDH protects the ischemic myocardium and alleviates diastolic dysfunction [ , ].

The hexosamine biosynthesis pathway HBP is another ancillary pathway of glycolysis capable of converting fructosephosphate FP and glutamine to glucosaminephosphate GlcN-6P via glutamine-fructosephosphate transaminase GFPT , and ultimately synthesizing riboside diphosphate N-acetylglucosamine UDP-GlcNAc.

There are two isoforms in humans, GFPT1 and GFPT2, with GFPT2 being the main type in the heart [ ]. UDP-GlcNAc is a substrate for a variety of biosynthetic pathways such as proteoglycans, hyaluronic acid, and glycolipids [ 12 ].

It also serves as a substrate for O-GlcNAc transferase OGT to O-GlcNAcylate proteins, which regulates cellular functions such as cell survival, signaling, and protein stability, and is thought to prevent cell death in response to stress [ , , ].

It has been found that increased post-translational O-GlcNA acylation due to HBP activation may be associated with systolic and diastolic dysfunction in diabetic cardiomyopathy [ ].

In addition, oxidative stress is an important risk factor in a variety of cardiovascular diseases, including diabetic cardiomyopathy, myocardial infarction, and heart failure. Oxidative stress has been reported to inhibit catalytic enzymes of the upstream pathway of glycolysis, including hexokinase, glyceraldehydephosphate dehydrogenase, and PFK, resulting in the accumulation of upstream intermediates e.

Increased fluxes of HBP play a dual role. Acute upregulation of HBP is cardioprotective. found that nuclear Tisp40, a membrane-resident transmembrane protein enriched in cardiomyocytes that is cleaved and released into the nucleus in response to ER stress, promotes HBP flux and protein O-GlcNAcylation by binding to the promoter of GFPT1, and is capable of attenuating myocardial injury in the ischemic heart [ ].

Chronic activation, however, can cause protein dysfunction through sustained elevation of protein O-GlcNAcylation, which ultimately leads to cardiovascular diseases such as diabetic cardiomyopathy, cardiac hypertrophy, ischemic cardiomyopathy, and heart failure [ ].

Tran et al. found that GFPT1 overexpression under hemodynamic stress caused upregulation of HBP, which subsequently induced heart failure and cardiac remodeling through persistent chronic activation of mTOR [ ].

U Rajamani et al. found that in diabetic patients, hyperglycemia activates HBP and leads to reduced BAD phosphorylation and BAD-Bcl2 dimer formation and accumulation, which mediates HBP-induced cardiomyocyte apoptosis and may be associated with myocardial contractile dysfunction during episodes of type 2 diabetes [ ].

The single-carbon metabolic pathway and the PPP pathway are the two main pathways for NADPH production in vivo. The activity of glucosephosphate dehydrogenase G6PD or G6PDH , the key rate-limiting enzyme of the PPP pathway, increases in response to oxidative stress stimulation, and the PPP pathway is up-regulated in response to stress overload, with some compensatory effects in early life [ , ].

In a study, it was noted that in the case of pressure overload-induced heart failure, there is a significant elevation of cardiac ROS, depletion of antioxidant defense mechanisms, and a decrease in the levels of NADPH the major antioxidant cofactor and GSH production [ ].

It also indicates that ATF4 a transcription factor can maintain NADPH homeostasis and cardiac function by directly controlling the expression of genes in the single-carbon metabolic pathway and the PPP, and has cardioprotective effects [ ].

In addition, Takao Kato et al. demonstrated that dichloroacetate improved CHF by increasing NADPH and GSH levels by activating the PPP and enhancing G6PD activity [ ].

In conclusion, activation of the PPP pathway and the single-carbon metabolic pathway attenuates oxidative stress in the myocardium and contributes to the improvement of HF. In ischemic heart disease, G6PD is required to maintain cellular GSH levels and prevent ischemia—reperfusion-induced myocardial injury [ ].

HBP and PPP can be tightly coupled through the O-GlcNAcylation of G6PD. Ou et al. found that hypoxic adaptation can further activate G6PD by using relevant inflammatory cytokines IL-6、IL-1β to increase O-GlcNAcylation in the heart and activate the HBP pathway.

Thus, O-GlcNA acylation of G6PD is promising as a new therapeutic target for ischemic heart disease. In addition, the PPP pathway was also found to be active during acute episodes of cardiac ischemia—reperfusion, and inhibition of PPP oxidation by ischemic preconditioning was able to reduce creatine kinase release and protect the heart from ischemic injury [ ].

PPP may also be involved in processes such as myocardial repair in patients with coronary heart disease and diabetes [ , ]. Recently, a study has found that PPP can act as a novel oxygen sensor and regulate hypoxic coronary artery diastole by modulating the activity of the SERCA to reduce intracellular calcium concentration.

However, whether this novel function works under various physiological and pathological conditions needs further investigation [ ].

In addition, the researchers found from cardiac progenitor cells CPCs of diabetic mice that key activities of the PPP pathway, G6PD, or transketolase were reduced and apoptosis was activated.

Re-PPP pathway using benfotiamine was able to rescue these CPCs [ ]. This indicates that the PPP pathway's activation may be a new therapeutic target to promote myocardial repair in diabetic patients. In normal and hypertrophied hearts, glucose from glycogen is preferentially oxidized relative to exogenous glucose.

Calcium overload may be an early event in LV dysfunction during reperfusion [ ]. Previous studies demonstrated that fasting protects the heart from ischemic injury by increasing glycogen utilization during ischemia [ ].

More recently, Mohamed et al. This limits LV dysfunction in early reperfusion injury, contributes to improved mitochondrial function and cell viability, and reduces infarct size [ ]. Similarly, ischemic preconditioning ameliorates myocardial ischemia by reducing the accumulation of glycolytic catabolic products by inhibiting glycogenolysis during sustained ischemia [ ].

Glycogen metabolism also has an important role in cardiac hypertrophy. It has been found that the overall rate of myocardial glycolysis increases in hypertrophied hearts during aerobic perfusion, but not during low-flow ischemia [ ].

Glycogen is an important source of glucose during low-flow ischemia, accounting for a significant percentage of the total rate of glycolysis. Not only that but the rate of glycogen renewal simultaneous synthesis and degradation is accelerated during severe low-flow ischemia [ , ].

D Mancini et al. showed that increasing the proportion of carbohydrates in the diet of patients with CHF exhaustion slowed the utilization of glycogen stores and improved exercise tolerance in CHF patients [ ]. The serine biosynthesis pathway is an auxiliary branch of the glycolytic pathway that allows for the de novo synthesis of serine using the glycolytic intermediate glyceraldehyde 3-phosphate G3P and its eventual conversion to glycine, which provides the carbon unit for single-carbon metabolism [ ].

The process involves three enzymes, phosphoglycerate dehydrogenase PHGDH , phosphoserine transaminase PSAT1 , and phosphoserine phosphorylase PSPH. Serine is an important nonessential amino acid involved in a variety of physiological processes and pathways.

For example, serine is a precursor to glycine and cysteine, and glycine is in turn a biosynthetic precursor to porphyrins. Serine is also involved in purine synthesis, sphingolipid, and phospholipid composition, and is essential for the biosynthesis of macromolecules required for cell proliferation [ 12 , ].

As a result, the serine biosynthesis pathway has received much attention in the field of cancer research. However, how this pathway functions in cardiovascular disease have not been addressed.

Recently, the serine biosynthetic pathway is associated with the onset and progression of hereditary dilated cardiomyopathy [ ]. This study found that activation of the ATF4-dependent serine biosynthesis pathway and TRIB4 kinase signaling using a specific combination of small molecule kinase inhibitors SMKIs was able to attenuate the dilated cardiomyopathy phenotype in iPSC-CMs by establishing a screening model for dilated cardiomyopathy iPSC-CMs, whereas inhibition of the serine biosynthesis biosynthetic pathway or PHGDH exacerbated contractile dysfunction in dilated cardiomyopathy iPSC-CMs.

suggesting that the serine biosynthesis pathway may have a cardioprotective role in dilated cardiomyopathy, but its specific link to dilated cardiomyopathy pathogenesis requires further investigation [ ].

In addition, Laura Padrón-Barthe et al. found that CnAβ1 was able to induce ATP synthesis and antioxidant metabolite production through activation of the sericinic acid pathway, resulting in a reduction of GSH production after pressure overload, with beneficial effects on reducing myocardial hypertrophy and improving cardiac function [ ].

Overall, activation of the serine biosynthesis pathway appears to be a favorable process for both cardiac physiology and pathophysiology and may serve as an important therapeutic target for cardiovascular disease in the future Fig.

Under hyperglycemic conditions, AR is activated and glucose metabolism is diverted to the Polyol bypass pathway. Activation of the PPP bypass pathway and the single-carbon pathway of metabolism increases the concentrations of NADPH and GSH, which maintain intracellular redox homeostasis and protect the heart.

Acute activation of the HBP pathway has a cardioprotective effect, and long-term chronic activation of the HBP pathway has a damaging effect on the heart; by inhibiting GSK-1, the HBP pathway is activated, and by inhibiting GSK-1, the HBP pathway is activated.

activation of the HBP pathway has a cardioprotective effect, and long-term chronic activation of the HBP pathway has a damaging effect on the heart.

Inhibition of GP partitioning by GSK-3 into the glycogen synthesis pathway reduces H production, intracellular acidosis, and calcium overload.

Improves mitochondrial function and protects the heart. Serine biosynthesis pathway is associated with the development of DCM. Specific activation of ATF4 using SMKI is able to activate the serine biosynthesis pathway through the activation of PHGDH and attenuate contractile dysfunction in DCM.

Cardiovascular disease CVD has a high prevalence worldwide and is the leading cause of death in China. With the prevalence of CVD, there is an urgent need to develop unconventional therapeutic tools to continuously improve the level of diagnosis and treatment of CVD. Over the past decades, it has been gradually discovered that glycolytic metabolism plays an indispensable role in several common CVD types e.

Although some of the mechanisms, including how glycolysis-related enzymes protect cardiac structure and function by regulating apoptosis in cardiomyocytes and inducing inducible mitochondrial autophagy, have been reported, the specific functions related to their multiple biological processes remain poorly defined.

In this review, we explored the relationship between glycolysis-related enzymes and CVD as much as possible. Among the ten enzymes related to glycolysis, HK is involved in myocardial ischemia—reperfusion and heart failure, PGI is involved in heart failure, PFK is involved in diastolic heart failure, diabetic cardiomyopathy, and coronary artery disease, ALDOA is involved in heart failure, myocardial infarction, arrhythmia, hypertrophic cardiomyopathy, and congenital heart disease and can be used as a serum marker for cardiogenic shock, PGAM is involved in heart failure, ischemia—reperfusion injury, and myocardial infarction, ENO is involved in heart failure, myocardial infarction, diabetic cardiomyopathy and Dox-induced myocardial injury, PKM is involved in myocardial infarction, heart failure, cardiomyopathy and atherosclerosis, and LDH is involved in post-infarction cardiac repair, heart failure and aortic dissection.

It is uncertain whether 3-phosphoglyceraldehyde dehydrogenase and phosphoglycerate kinase are involved in CVD. The auxiliary pathways of glycolysis polyol pathway, pentose phosphate pathway, single-carbon metabolism, hexosamine biosynthesis pathway, glycogen metabolism, and serine biosynthesis pathway also play important roles in CVD.

Mechanisms that have been demonstrated in studies of glycolysis-related enzymes include that binding of HK2 to VDAC on the outer mitochondrial membrane inhibits the opening of mPTP and reduces cell death, and that mTORC1-mediated modulation of mitochondrial autophagy promotes mitochondrial homeostasis and reduces the extent of myocardial injury during ischemia—reperfusion.

Inhibition of the RIP3-PGAM5-Drp1-mitochondrial pathway was able to achieve myocardial protection by inhibiting necrotic apoptosis. Inhibition of transcriptional activation of ENO1 was able to reduce glycolysis and prevent myocardial fibrosis after MI, among others.

It is important to note that most of the signaling pathways and mechanisms identified in these studies were performed in mouse and cellular models, and it is uncertain whether they are equally applicable to human patient tissues.

Similarly, activators and inhibitors of the relevant targets have not been tested in clinical trials, and more work is needed to apply basic research findings to clinical settings.

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Thank you for visiting Glucose metabolism pathways disorders. You Enhance cognitive skills using a Disordegs version Gludose limited support patyways CSS. To obtain the Glucose metabolism pathways disorders experience, we disofders you Glucose metabolism pathways disorders a more up to date Chronic pain treatment or turn off compatibility mode in Internet Explorer. In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript. In mammals, the white adipocyte is a cell type that is specialized for storage of energy in the form of triacylglycerols and for energy mobilization as fatty acids. White adipocyte metabolism confers an essential role to adipose tissue in whole-body homeostasis. Chronic pain treatment disorders are conditions that affect any aspect Glucosw metabolism. Psthways can include tiredness, weight loss or gain, and pathwaays and Glucose metabolism pathways disorders. Metabolism Beauty from within a term that describes the biochemical processes that allow people to grow, reproduce, repair damage, and respond to their environment. A metabolic disorder is a condition that impairs these processes. For example, it could affect the availability of enzymes for breaking down food or how efficiently cells can produce energy.

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