Category: Home

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.

Symptoms and outlook vary widely. It normally affects the spleen first. My podcast changed me Can 'biological race' explain disparities in health? Why Parkinson's research is zooming in on the gut Tools General Health Drugs A-Z Health Hubs Health Tools Find a Doctor BMI Calculators and Charts Blood Pressure Chart: Ranges and Guide Breast Cancer: Self-Examination Guide Sleep Calculator Quizzes RA Myths vs Facts Type 2 Diabetes: Managing Blood Sugar Ankylosing Spondylitis Pain: Fact or Fiction Connect About Medical News Today Who We Are Our Editorial Process Content Integrity Conscious Language Newsletters Sign Up Follow Us.

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.

Metabolic disorder definition. Common metabolic disorders. Common symptoms. Treatment options. When to see a doctor. 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. Share this article. Latest news Ovarian tissue freezing may help delay, and even prevent menopause. RSV vaccine errors in babies, pregnant people: Should you be worried?

Scientists discover biological mechanism of hearing loss caused by loud noise — and find a way to prevent it. How gastric bypass surgery can help with type 2 diabetes remission.

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.

Andersson C, Vasan RS Epidemiology of cardiovascular disease in young individuals. Nat Rev Cardiol — Article PubMed Google Scholar. Steven S, Frenis K, Oelze M, Kalinovic S, Kuntic M, Bayo Jimenez MT, Vujacic-Mirski K, Helmstädter J, Kröller-Schön S, Münzel T, Daiber A Vascular inflammation and oxidative stress: major triggers for cardiovascular disease.

Oxid Med Cell Longev Article CAS PubMed PubMed Central Google Scholar. Soppert J, Lehrke M, Marx N, Jankowski J, Noels H Lipoproteins and lipids in cardiovascular disease: from mechanistic insights to therapeutic targeting.

Adv Drug Deliv Rev — Article CAS PubMed Google Scholar. Sunkara A, Raizner A Supplemental vitamins and minerals for cardiovascular disease prevention and treatment.

Methodist Debakey Cardiovasc J — Article PubMed PubMed Central Google Scholar. Zhao D, Liu J, Wang M, Zhang X, Zhou M Epidemiology of cardiovascular disease in China: current features and implications.

Zhou Y, Song K, Tu B, Sun H, Ding JF, Luo Y, Sha JM, Li R, Zhang Y, Zhao JY, Tao H METTL3 boosts glycolysis and cardiac fibroblast proliferation by increasing AR methylation.

Int J Biol Macromol — Mol Med Rep — Chang YC, Kim CH Molecular research of glycolysis. Int J Mol Sci. Feng J, Li J, Wu L, Yu Q, Ji J, Wu J, Dai W, Guo C Emerging roles and the regulation of aerobic glycolysis in hepatocellular carcinoma.

J Exp Clin Cancer Res TeSlaa T, Bartman CR, Jankowski CSR, Zhang Z, Xu X, Xing X, Wang L, Lu W, Hui S, Rabinowitz JD The source of glycolytic intermediates in mammalian tissues. Cell Metab Badolia R, Ramadurai DKA, Abel ED, Ferrin P, Taleb I, Shankar TS, Krokidi AT, Navankasattusas S, McKellar SH, Yin M, Kfoury AG, Wever-Pinzon O, Fang JC, Selzman CH, Chaudhuri D, Rutter J, Drakos SG The role of nonglycolytic glucose metabolism in myocardial recovery upon mechanical unloading and circulatory support in chronic heart failure.

Circulation — Tran DH, Wang ZV Glucose metabolism in cardiac hypertrophy and heart failure. J Am Heart Assoc 8:e Brahma MK, Pepin ME, Wende AR My sweetheart is broken: role of glucose in diabetic cardiomyopathy. Diabetes Metab J —9. Lopaschuk GD, Karwi QG, Tian R, Wende AR, Abel ED Cardiac energy metabolism in heart failure.

Circ Res — Bertero E, Maack C Metabolic remodelling in heart failure. Calmettes G, Ribalet B, John S, Korge P, Ping P, Weiss JN Hexokinases and cardioprotection.

J Mol Cell Cardiol — John S, Weiss JN, Ribalet B Subcellular localization of hexokinases I and II directs the metabolic fate of glucose. PLoS ONE 6:e Depre C, Vanoverschelde JL, Taegtmeyer H Glucose for the heart. Wu R, Wyatt E, Chawla K, Tran M, Ghanefar M, Laakso M, Epting CL, Ardehali H Hexokinase II knockdown results in exaggerated cardiac hypertrophy via increased ROS production.

EMBO Mol Med — Rabbani N, Xue M, Thornalley PJ Hexokinaselinked glycolytic overload and unscheduled glycolysis-driver of insulin resistance and development of vascular complications of diabetes. Rabbani N, Thornalley PJ Hexokinase-2 glycolytic overload in diabetes and ischemia-reperfusion injury.

Trends Endocrinol Metab — Free Radic Biol Med — Lemasters JJ, Holmuhamedov E Voltage-dependent anion channel VDAC as mitochondrial governator—thinking outside the box.

Biochim Biophys Acta — Pasdois P, Parker JE, Halestrap AP Extent of mitochondrial hexokinase II dissociation during ischemia correlates with mitochondrial cytochrome c release, reactive oxygen species production, and infarct size on reperfusion.

J Am Heart Assoc 2:e Kim KW, Kim SW, Lim S, Yoo KJ, Hwang KC, Lee S Neutralization of hexokinase 2-targeting miRNA attenuates the oxidative stress-induced cardiomyocyte apoptosis. Clin Hemorheol Microcirc — Halestrap AP, Pereira GC, Pasdois P The role of hexokinase in cardioprotection - mechanism and potential for translation.

Br J Pharmacol — Nederlof R, Eerbeek O, Hollmann MW, Southworth R, Zuurbier CJ Targeting hexokinase II to mitochondria to modulate energy metabolism and reduce ischaemia-reperfusion injury in heart.

Guo L Mitochondrial ATP synthase inhibitory factor 1 interacts with the pcyclophilin D complex and promotes opening of the permeability transition pore. J Biol Chem Guo L Mitochondria and the permeability transition pore in cancer metabolic reprogramming.

Biochem Pharmacol Ciscato F, Ferrone L, Masgras I, Laquatra C, Rasola A Hexokinase 2 in Cancer: A Prima Donna Playing Multiple Characters. Murry CE, Jennings RB, Reimer KA Preconditioning with ischemia: a delay of lethal cell injury in ischemic myocardium. Eur J Pharmacol — Gürel E, Smeele KM, Eerbeek O, Koeman A, Demirci C, Hollmann MW, Zuurbier CJ Ischemic preconditioning affects hexokinase activity and HKII in different subcellular compartments throughout cardiac ischemia-reperfusion.

J Appl Physiol — Article CAS Google Scholar. Zuurbier CJ, Eerbeek O, Meijer AJ Ischemic preconditioning, insulin, and morphine all cause hexokinase redistribution. Am J Physiol Heart Circ Physiol H—H Zuurbier CJ, Bertrand L, Beauloye CR, Andreadou I, Ruiz-Meana M, Jespersen NR, Kula-Alwar D, Prag HA, Eric Botker H, Dambrova M, Montessuit C, Kaambre T, Liepinsh E, Brookes PS, Krieg T Cardiac metabolism as a driver and therapeutic target of myocardial infarction.

J Cell Mol Med — Cell Cycle — Sun J, Mishra J, Yang M, Stowe DF, Heisner JS, An J, Kwok WM, Camara AKS Hypothermia Prevents Cardiac Dysfunction during Acute Ischemia Reperfusion by Maintaining Mitochondrial Bioenergetics and by Promoting Hexokinase II Binding to Mitochondria.

J Pineal Res. Yang M, Xu Y, Heisner JS, Sun J, Stowe DF, Kwok WM, Camara AKS Peroxynitrite nitrates adenine nucleotide translocase and voltage-dependent anion channel 1 and alters their interactions and association with hexokinase II in mitochondria. Mitochondrion — J Physiol Biochem — Smeele KM, Southworth R, Wu R, Xie C, Nederlof R, Warley A, Nelson JK, van Horssen P, van den Wijngaard JP, Heikkinen S, Laakso M, Koeman A, Siebes M, Eerbeek O, Akar FG, Ardehali H, Hollmann MW, Zuurbier CJ Disruption of hexokinase II-mitochondrial binding blocks ischemic preconditioning and causes rapid cardiac necrosis.

Ajoolabady A, Chiong M, Lavandero S, Klionsky DJ, Ren J Mitophagy in cardiovascular diseases: molecular mechanisms, pathogenesis, and treatment.

Trends Mol Med — Popov SV, Mukhomedzyanov AV, Voronkov NS, Derkachev IA, Boshchenko AA, Fu F, Sufianova GZ, Khlestkina MS, Maslov LN Regulation of autophagy of the heart in ischemia and reperfusion. Apoptosis — Zhu J, Wang H, Jiang X mTORC1 beyond anabolic metabolism: Regulation of cell death.

J Cell Biol. Autophagy — Tan VP, Smith JM, Tu M, Yu JD, Ding EY, Miyamoto S Dissociation of mitochondrial HK-II elicits mitophagy and confers cardioprotection against ischemia.

Cell Death Dis Beltran C, Pardo R, Bou-Teen D, Ruiz-Meana M, Villena JA, Ferreira-González I, Barba I Enhancing Glycolysis Protects against Ischemia-Reperfusion Injury by Reducing ROS Production. Wan Q, Kong D, Liu Q, Guo S, Wang C, Zhao Y, Ke ZJ, Yu Y Congestive heart failure in COX2 deficient rats.

Sci China Life Sci — McCommis KS, Douglas DL, Krenz M, Baines CP Cardiac-specific hexokinase 2 overexpression attenuates hypertrophy by increasing pentose phosphate pathway flux.

Moc C, Taylor AE, Chesini GP, Zambrano CM, Barlow MS, Zhang X, Gustafsson B, Å, and NH Purcell, Physiological activation of Akt by PHLPP1 deletion protects against pathological hypertrophy. Cardiovasc Res — Yuan C, Wu Z, Jin C, Cao W, Dong Y, Chen J, Liu C Qiangxin recipe improves doxorubicin-induced chronic heart failure by enhancing KLF5-mediated glucose metabolism.

Phytomedicine Uthman L, Kuschma M, Römer G, Boomsma M, Kessler J, Hermanides J, Hollmann MW, Preckel B, Zuurbier CJ, Weber NC Novel anti-inflammatory effects of canagliflozin involving hexokinase II in lipopolysaccharide-stimulated human coronary artery endothelial cells.

Cardiovasc Drugs Ther — Kedar PS, Dongerdiye R, Chilwirwar P, Gupta V, Chiddarwar A, Devendra R, Warang P, Prasada H, Sampagar A, Bhat S, Chandrakala S, Madkaikar M Glucose phosphate isomerase deficiency: high prevalence of p. ArgHis mutation in Indian population associated with severe hereditary non-spherocytic hemolytic anemia coupled with neurological dysfunction.

Indian J Pediatr — Finelli MJ, Paramo T, Pires E, Ryan BJ, Wade-Martins R, Biggin PC, McCullagh J, Oliver PL Oxidation resistance 1 modulates glycolytic pathways in the cerebellum via an interaction with glucosephosphate isomerase. Mol Neurobiol — Karlstaedt A, Khanna R, Thangam M, Taegtmeyer H Glucose 6-phosphate accumulates via phosphoglucose isomerase inhibition in heart muscle.

Davogustto GE, Salazar RL, Vasquez HG, Karlstaedt A, Dillon WP, Guthrie PH, Martin JR, Vitrac H, De La Guardia G, Vela D, Ribas-Latre A, Baumgartner C, Eckel-Mahan K, Taegtmeyer H Metabolic remodeling precedes mTORC1-mediated cardiac hypertrophy.

Meloni L, Manca MR, Loddo I, Cioglia G, Cocco P, Schwartz A, Muntoni S, Muntoni S Glucosephosphate dehydrogenase deficiency protects against coronary heart disease. J Inherit Metab Dis — Zhang Y, Zhao H, Liu B, Li L, Zhang L, Bao M, Ji X, He X, Yi J, Chen P, Lu C, Lu A Low level antibodies against alpha-tropomyosin are associated with increased risk of coronary heart disease.

Front Pharmacol van Boekel MA, Vossenaar ER, van den Hoogen FH, van Venrooij WJ Autoantibody systems in rheumatoid arthritis: specificity, sensitivity and diagnostic value. Arthritis Res — Mor I, Cheung EC, Vousden KH Control of glycolysis through regulation of PFK1: old friends and recent additions.

Cold Spring Harb Symp Quant Biol — Wang J, Xu J, Wang Q, Brainard RE, Watson LJ, Jones SP, Epstein PN Reduced cardiac fructose 2,6 bisphosphate increases hypertrophy and decreases glycolysis following aortic constriction. PLoS ONE 8:e Int Heart J — da Silva RC, Polegato BF, Azevedo PS, Fernandes AA, Okoshi K, de Paiva SAR, Minicucci MF, Zornoff LAM Jaboticaba Myrciaria jaboticaba attenuates ventricular remodeling after myocardial infarction in rats.

Potente M, Carmeliet P The link between angiogenesis and endothelial metabolism. Annu Rev Physiol — Vigil-Garcia M, Demkes CJ, Eding JEC, Versteeg D, de Ruiter H, Perini I, Kooijman L, Gladka MM, Asselbergs FW, Vink A, Harakalova M, Bossu A, van Veen TAB, Boogerd CJ, van Rooij E Gene expression profiling of hypertrophic cardiomyocytes identifies new players in pathological remodelling.

He X, Zeng H, Cantrell AC, Chen JX Regulatory role of TIGAR on endothelial metabolism and angiogenesis. J Cell Physiol — He X, Zeng H, Cantrell AC, Williams QA, Chen JX Knockout of TIGAR enhances myocardial phosphofructokinase activity and preserves diastolic function in heart failure.

He X, Cantrell AC, Williams QA, Gu W, Chen Y, Chen JX, Zeng H P53 acetylation exerts critical roles in pressure overload induced coronary microvascular dysfunction and heart failure.

Bockus LB, Matsuzaki S, Vadvalkar SS, Young ZT, Giorgione JR, Newhardt MF, Kinter M, Humphries KM Cardiac insulin signaling regulates glycolysis through phosphofructokinase 2 content and activity. J Am Heart Assoc. J Biol Chem — Cellular basis of insulin insensitivity in large rat adipocytes.

CAS PubMed PubMed Central Google Scholar. Cushman, S. Potential mechanism of insulin action on glucose transport in the isolated rat adipose cell. Apparent translocation of intracellular transport systems to the plasma membrane. Suzuki, K. Evidence that insulin causes translocation of glucose transport activity to the plasma membrane from an intracellular storage site.

Natl Acad. USA 77 , — Hotamisligil, G. Adipose expression of tumor necrosis factor-alpha: direct role in obesity-linked insulin resistance. Science , 87—91 Hu, E. AdipoQ is a novel adipose-specific gene dysregulated in obesity.

Maeda, K. et al. cDNA cloning and expression of a novel adipose specific collagen-like factor, apM1 AdiPose Most abundant Gene transcript 1. Scherer, P. A novel serum protein similar to C1q, produced exclusively in adipocytes. Zhang, Y. Positional cloning of the mouse obese gene and its human homologue.

Nature , — Lafontan, M. Historical perspectives in fat cell biology: the fat cell as a model for the investigation of hormonal and metabolic pathways. Cell Physiol. Guilherme, A. Molecular pathways linking adipose innervation to insulin action in obesity and diabetes mellitus. Chouchani, E. Metabolic adaptation and maladaptation in adipose tissue.

PubMed PubMed Central Google Scholar. Scheja, L. The endocrine function of adipose tissues in health and cardiometabolic disease. Vishvanath, L. Contribution of adipogenesis to healthy adipose tissue expansion in obesity.

Ghaben, A. Adipogenesis and metabolic health. Cell Biol. Stenkula, K. Adipose cell size: importance in health and disease. Physiol , R—R Engfeldt, P. Lipolysis in human adipocytes, effects of cell size, age and of regional differences.

Laforest, S. Adipocyte size as a determinant of metabolic disease and adipose tissue dysfunction. Pausova, Z. From big fat cells to high blood pressure: a pathway to obesity-associated hypertension.

PubMed Google Scholar. Arner, P. Fat cell turnover in humans. Tandon, P. Adipose morphology and metabolic disease. Rutkowski, J. The cell biology of fat expansion. Berry, R. Weighing in on adipocyte precursors. Cell Metab.

Christodoulides, C. Adipogenesis and WNT signalling. Trends Endocrinol. Ma, X. Deciphering the roles of PPARγ in adipocytes via dynamic change of transcription complex.

Google Scholar. Shan, T. Roles of notch signaling in adipocyte progenitor cells and mature adipocytes. Fernando, R. Low steady-state oxidative stress inhibits adipogenesis by altering mitochondrial dynamics and decreasing cellular respiration.

Redox Biol. Wang, S. Sakaguchi, M. Adipocyte dynamics and reversible metabolic syndrome in mice with an inducible adipocyte-specific deletion of the insulin receptor.

Wang, Q. Reversible de-differentiation of mature white adipocytes into preadipocyte-like precursors during lactation. e3 Sebo, Z. Assembling the adipose organ: adipocyte lineage segregation and adipogenesis in vivo. Development , dev Raajendiran, A.

Identification of metabolically distinct adipocyte progenitor cells in human adipose tissues. Cell Rep. e7 Gavin, K. De novo generation of adipocytes from circulating progenitor cells in mouse and human adipose tissue. FASEB J. Ryden, M.

Adipocyte triglyceride turnover and lipolysis in lean and overweight subjects. Lipid Res. Walker, G. The pathophysiology of abdominal adipose tissue depots in health and disease. Hoffstedt, J. Regional impact of adipose tissue morphology on the metabolic profile in morbid obesity.

Diabetologia 53 , — Veilleux, A. Visceral adipocyte hypertrophy is associated with dyslipidemia independent of body composition and fat distribution in women. Diabetes 60 , — Verboven, K. Abdominal subcutaneous and visceral adipocyte size, lipolysis and inflammation relate to insulin resistance in male obese humans.

Lonn, M. Adipocyte size predicts incidence of type 2 diabetes in women. Weyer, C. Enlarged subcutaneous abdominal adipocyte size, but not obesity itself, predicts type II diabetes independent of insulin resistance.

Diabetologia 43 , — White, U. Dynamics of adipose tissue turnover in human metabolic health and disease. Diabetologia 62 , 17—23 Spalding, K. Retrospective birth dating of cells in humans. Cell , — Dynamics of fat cell turnover in humans.

Arner, E. Adipocyte turnover: relevance to human adipose tissue morphology. Diabetes 59 , — Dynamics of human adipose lipid turnover in health and metabolic disease.

This study provides the first in vivo estimation of TAG renewal rate in adult human adipose tissue. Guillermier, C. Imaging mass spectrometry demonstrates age-related decline in human adipose plasticity. JCI Insight 2 , e Impact of fat mass and distribution on lipid turnover in human adipose tissue.

Ibrahim, M. Subcutaneous and visceral adipose tissue: structural and functional differences. Lee, M. Adipose tissue heterogeneity: implication of depot differences in adipose tissue for obesity complications.

CAS Google Scholar. Adipose lipid turnover and long-term changes in body weight. Kersten, S. Physiological regulation of lipoprotein lipase. Acta , — Thompson, B. Cell Endocrinol. Coleman, R. Mammalian triacylglycerol metabolism: synthesis, lipolysis, and signaling.

It takes a village: channeling fatty acid metabolism and triacylglycerol formation via protein interactomes. Chitraju, C. The triglyceride synthesis enzymes DGAT1 and DGAT2 have distinct and overlapping functions in adipocytes. Triglyceride synthesis by DGAT1 protects adipocytes from lipid-induced ER Stress during lipolysis.

Solinas, G. De novo lipogenesis in metabolic homeostasis: More friend than foe? This review questions the classical view of de novo lipogenesis as a detrimental pathway. Wallace, M. Tracing insights into de novo lipogenesis in liver and adipose tissues.

Cell Dev. Zhao, S. ATP-citrate lyase controls a glucose-to-acetate metabolic switch. Guillou, H. The key roles of elongases and desaturases in mammalian fatty acid metabolism: Insights from transgenic mice.

Aarsland, A. Hepatic and whole-body fat synthesis in humans during carbohydrate overfeeding. Diraison, F. Differences in the regulation of adipose tissue and liver lipogenesis by carbohydrates in humans. Smith, G. Insulin resistance drives hepatic de novo lipogenesis in nonalcoholic fatty liver disease.

Lipolysis and lipid mobilization in human adipose tissue. Morigny, P. Adipocyte lipolysis and insulin resistance.

Biochimie , — Langin, D. Importance of TNFα and neutral lipases in human adipose tissue lipolysis. Haemmerle, G. Defective lipolysis and altered energy metabolism in mice lacking adipose triglyceride lipase. Science , — Ahmadian, M. Schoiswohl, G. Impact of reduced ATGL-mediated adipocyte lipolysis on obesity-associated insulin resistance and inflammation in male mice.

Endocrinology , — Bezaire, V. Contribution of adipose triglyceride lipase and hormone-sensitive lipase to lipolysis in hMADS adipocytes.

Fischer, J. The gene encoding adipose triglyceride lipase PNPLA2 is mutated in neutral lipid storage disease with myopathy.

Natali, A. Metabolic consequences of adipose triglyceride lipase deficiency in humans: an in vivo study in patients with neutral lipid storage disease with myopathy. Hormone-sensitive lipase deficiency in mice causes diglyceride accumulation in adipose tissue, muscle, and testis.

Albert, J. Null mutation in hormone-sensitive lipase gene and risk of type 2 diabetes. Taschler, U. Monoglyceride lipase deficiency in mice impairs lipolysis and attenuates diet-induced insulin resistance. Lass, A. Adipose triglyceride lipase-mediated lipolysis of cellular fat stores is activated by CGI and defective in Chanarin-Dorfman syndrome.

Radner, F. Growth retardation, impaired triacylglycerol catabolism, hepatic steatosis, and lethal skin barrier defect in mice lacking comparative gene identification CGI El-Assaad, W. Diabetologia 58 , — Yang, X. Grahn, T. Fat-specific protein 27 FSP27 interacts with adipose triglyceride lipase ATGL to regulate lipolysis and insulin sensitivity in human adipocytes.

Nishino, N. FSP27 contributes to efficient energy storage in murine white adipocytes by promoting the formation of unilocular lipid droplets.

Granneman, J. Perilipin controls lipolysis by regulating the interactions of AB-hydrolase containing 5 Abhd5 and adipose triglyceride lipase Atgl. Wang, H. Activation of hormone-sensitive lipase requires two steps, protein phosphorylation and binding to the PAT-1 domain of lipid droplet coat proteins.

Shen, W. Characterization of the functional interaction of adipocyte lipid-binding protein with hormone-sensitive lipase. Smith, A. Physical association between the adipocyte fatty acid-binding protein and hormone-sensitive lipase: a fluorescence resonance energy transfer analysis.

Aboulaich, N. Association and insulin regulated translocation of hormone-sensitive lipase with PTRF. Zhou, S. Acetylation of cavin-1 promotes lipolysis in white adipose tissue. Nordstrom, E. A human-specific role of cell death-inducing DFFA DNA fragmentation factor-alpha -like effector A CIDEA in adipocyte lipolysis and obesity.

Diabetes 54 , — Puri, V. Cidea is associated with lipid droplets and insulin sensitivity in humans. USA , — Jash, S. CIDEA transcriptionally regulates UCP1 for britening and thermogenesis in human fat cells. iScience 20 , 73—89 Kulyte, A. CIDEA interacts with liver X receptors in white fat cells.

FEBS Lett. Wang, W. Cidea is an essential transcriptional coactivator regulating mammary gland secretion of milk lipids. Zhang, C. The new face of the lipid droplet: lipid droplet proteins. Proteomics 19 , e Lizaso, A. beta-adrenergic receptor-stimulated lipolysis requires the RAB7-mediated autolysosomal lipid degradation.

Autophagy 9 , — Singh, R. Autophagy regulates adipose mass and differentiation in mice. Adipose-specific deletion of autophagy-related gene 7 atg7 in mice reveals a role in adipogenesis. Flaherty, S. A lipase-independent pathway of lipid release and immune modulation by adipocytes.

Eissing, L. De novo lipogenesis in human fat and liver is linked to ChREBP-β and metabolic health. Herman, M. A novel ChREBP isoform in adipose tissue regulates systemic glucose metabolism.

This study describes a new adipose isoform of the transcription factor ChREBP that is positively associated with insulin sensitivity. Kursawe, R. Diabetes 62 , — Interaction between hormone-sensitive lipase and ChREBP in fat cells controls insulin sensitivity.

This study shows the unexpected role of an adipocyte metabolic enzyme as a modulator of transcription factor activity. Collins, J. De novo lipogenesis and stearoyl-CoA desaturase are coordinately regulated in the human adipocyte and protect against palmitate-induced cell injury. Adipocyte lipid synthesis coupled to neuronal control of thermogenic programming.

Neuronal modulation of brown adipose activity through perturbation of white adipocyte lipogenesis. Sukonina, V. FOXK1 and FOXK2 regulate aerobic glycolysis. DiGirolamo, M. Lactate production in adipose tissue: a regulated function with extra-adipose implications.

Jansson, P. Lactate release from the subcutaneous tissue in lean and obese men. Krycer, J. Lactate production is a prioritized feature of adipocyte metabolism.

Hui, S. Glucose feeds the TCA cycle via circulating lactate. Rabinowitz, J. Lactate: the ugly duckling of energy metabolism. Lee, K. Developmental and functional heterogeneity of white adipocytes within a single fat depot.

EMBO J. Tbx15 defines a glycolytic subpopulation and white adipocyte heterogeneity. Diabetes 66 , — Luong, Q. Deciphering white adipose tissue heterogeneity.

Biology 8 , 23 CAS PubMed Central Google Scholar. Lynes, M. Deciphering adipose tissue heterogeneity. Newsholme, E. Substrate cycles in metabolic regulation and in heat generation.

Sanchez-Gurmaches, J. Emerging complexities in adipocyte origins and identity. Trends Cell Biol. Harms, M. Mature human white adipocytes cultured under membranes maintain identity, function, and can transdifferentiate into brown-like adipocytes. e5 Kroon, T. PPARγ and PPARα synergize to induce robust browning of white fat in vivo.

Tiraby, C. Acquirement of brown fat cell features by human white adipocytes. Control of brown and beige fat development. Pisani, D.

Barquissau, V. White-to-brite conversion in human adipocytes promotes metabolic reprogramming towards fatty acid anabolic and catabolic pathways.

Mills, E. Accumulation of succinate controls activation of adipose tissue thermogenesis. Murphy, M. Krebs cycle reimagined: the emerging roles of succinate and itaconate as signal transducers.

Kotzbeck, P. Brown adipose tissue whitening leads to brown adipocyte death and adipose tissue inflammation. Roh, H. Warming induces significant reprogramming of beige, but not brown, adipocyte cellular identity. This study describes the epigenomic control of the interconversion between beige and white adipocytes.

Inagaki, T. Histone demethylases regulate adipocyte thermogenesis. Duteil, D. LSD1 promotes oxidative metabolism of white adipose tissue. Sambeat, A. LSD1 Interacts with Zfp to promote UCP1 transcription and brown fat program. Zeng, X. Lysine-specific demethylase 1 promotes brown adipose tissue thermogenesis via repressing glucocorticoid activation.

Genes Dev. Guan, H. A futile metabolic cycle activated in adipocytes by antidiabetic agents. Mazzucotelli, A. The transcriptional coactivator peroxisome proliferator activated receptor PPAR γ coactivator-1α and the nuclear receptor PPARα control the expression of glycerol kinase and metabolism genes independently of PPARγ activation in human white adipocytes.

Diabetes 56 , — Flachs, P. Induction of lipogenesis in white fat during cold exposure in mice: link to lean phenotype.

Ikeda, K. UCP1-independent signaling involving SERCA2b-mediated calcium cycling regulates beige fat thermogenesis and systemic glucose homeostasis.

New advances in adaptive thermogenesis: UCP1 and beyond. Kazak, L. A creatine-driven substrate cycle enhances energy expenditure and thermogenesis in beige fat. Bertholet, A. Mitochondrial Patch clamp of beige adipocytes reveals UCP1-positive and UCP1-negative cells both exhibiting futile creatine cycling.

e4 Ablation of adipocyte creatine transport impairs thermogenesis and causes diet-induced obesity. Pollard, A. AMPK activation protects against diet induced obesity through Ucp1-independent thermogenesis in subcutaneous white adipose tissue.

Mottillo, E. Coupling of lipolysis and de novo lipogenesis in brown, beige, and white adipose tissues during chronic β3-adrenergic receptor activation.

Girousse, A. Partial inhibition of adipose tissue lipolysis improves glucose metabolism and insulin sensitivity without alteration of fat mass. PLoS Biol. Newgard, C.

A branched-chain amino acid-related metabolic signature that differentiates obese and lean humans and contributes to insulin resistance. White, P. Branched-chain amino acids in disease. Lotta, L. Genetic predisposition to an impaired metabolism of the branched-chain amino acids and risk of type 2 diabetes: a mendelian randomisation analysis.

PLoS Med. Klimcakova, E.

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.

Author: Dourg

1 thoughts on “Glucose metabolism pathways disorders

Leave a comment

Yours email will be published. Important fields a marked *

Design by ThemesDNA.com