The relationship between alcohol consumption and carbohydrate metabolism is complex and is not fully understood. Alcohol not only increases oxidative stress during metabolism, but also inhibits both gluconeogenesis and glycogenolysis in liver. Thus, acute alcohol intake can lead to hypoglycemia, particularly when glycogen stores are depleted or when alcohol is taken without meals. In addition, carbohydrate-rich food taken together with alcohol exaggerates insulin secretion and can cause reactive hypoglycemia about 2 to 3 hours after the meal. It is well established that mild to moderate alcohol consumption (3 drinks/day) is associated with reduced cardiovascular mortality through improvements in insulin sensitivity, lipid profiles, and blood pressure. These beneficial effects of alcohol may also be responsible for a decreased incidence of type 2 diabetes mellitus (T2DM) and a reduced risk of coronary heart disease (CHD) in patients with T2DM. However, excessive alcohol consumption causes higher insulin resistance and increases the risk of T2DM, and even reverses the favorable effects of moderate alcohol intake on CHD.
Alcohol Drinking ; Alcohols ; Blood Pressure ; Carbohydrate Metabolism ; Coronary Disease ; Diabetes Mellitus ; Diabetes Mellitus, Type 2 ; Gluconeogenesis ; Glucose ; Glycogen ; Glycogenolysis ; Humans ; Hypoglycemia ; Incidence ; Insulin ; Insulin Resistance ; Liver ; Meals ; Oxidative Stress

In anesthetized normocapnic and normotensive dogs, the effect of arterial hypoxemia on cerebral blood flow and oxidative carbohydrate metabolism was studied. The results are as follows: 1) The hypoxic vasodilatory effect on cerevral vessels is intact even at profound systemic hypoxemia(Pao2 30 torr) if Paco2 is controlled within normal limits. 2) CMRO2 did not significantly increase above the normal even during profound arterial hopoxemis, indicating that CMRO2 levels are poor indices of hypoxia. 3) A disporportinately high glycolysis at Pao2 of 50 torr suggested early cerebral metabolic changes which became more marked with further decrease in Pao2. 4) One hour after restitution of normoxia, however, carebral blood flow and metabolism manifested complete recovery. 6) It is concluded that a transient(20 minutes) profoun systemic arterial hypoxemia does not produce prolonged disorder of cerebral blood flow and oxidative carbohydrate metabolism provided that the cerebral perfusion pressure is kept normal.
Animals ; Anoxia* ; Carbohydrate Metabolism ; Cerebrovascular Circulation* ; Dogs ; Glycolysis ; Metabolism*

Biomass carbohydrates assimilation and lipid accumulation by Mortierella isabellina M2 strain were investigated. Corn fiber hydrolysate was specially studied. The results showed M. isabellina M2 strain achieved growth and lipid accumulation while glucose, xylose, mannose and arabinose were introduced as single carbon source, respectively. When M. isabellina M2 strain was cultivated on corn fiber hydrolysate with 6% sugars concentration, the biomass reached 18.2 g/L, the lipid content of dry mycelia was 45.7%, and the lipid yield achieved 8.3 g/L. It provided a promising perspective for microbial oils production with biomass hydrolysates.
Biomass ; Carbohydrate Metabolism ; Carbon ; metabolism ; Fermentation ; Industrial Microbiology ; methods ; Lipids ; biosynthesis ; Mortierella ; metabolism ; Zea mays ; metabolism

Energy metabolism is significantly reprogrammed in many human cancers, and these alterations confer many advantages to cancer cells, including the promotion of biosynthesis, ATP generation, detoxification and support of rapid proliferation. The pentose phosphate pathway (PPP) is a major pathway for glucose catabolism. The PPP directs glucose flux to its oxidative branch and produces a reduced form of nicotinamide adenine dinucleotide phosphate (NADPH), an essential reductant in anabolic processes. It has become clear that the PPP plays a critical role in regulating cancer cell growth by supplying cells with not only ribose-5-phosphate but also NADPH for detoxification of intracellular reactive oxygen species, reductive biosynthesis and ribose biogenesis. Thus, alteration of the PPP contributes directly to cell proliferation, survival and senescence. Furthermore, recent studies have shown that the PPP is regulated oncogenically and/or metabolically by numerous factors, including tumor suppressors, oncoproteins and intracellular metabolites. Dysregulation of PPP flux dramatically impacts cancer growth and survival. Therefore, a better understanding of how the PPP is reprogrammed and the mechanism underlying the balance between glycolysis and PPP flux in cancer will be valuable in developing therapeutic strategies targeting this pathway.
Animals ; Energy Metabolism ; Glucose ; metabolism ; Glycolysis ; Humans ; Neoplasms ; metabolism ; pathology ; Pentose Phosphate Pathway ; physiology

Glucose homeostasis is tightly regulated to meet the energy requirements of the vital organs and maintain an individual's health. The liver has a major role in the control of glucose homeostasis by controlling various pathways of glucose metabolism, including glycogenesis, glycogenolysis, glycolysis and gluconeogenesis. Both the acute and chronic regulation of the enzymes involved in the pathways are required for the proper functioning of these complex interwoven systems. Allosteric control by various metabolic intermediates, as well as post-translational modifications of these metabolic enzymes constitute the acute control of these pathways, and the controlled expression of the genes encoding these enzymes is critical in mediating the longer-term regulation of these metabolic pathways. Notably, several key transcription factors are shown to be involved in the control of glucose metabolism including glycolysis and gluconeogenesis in the liver. In this review, we would like to illustrate the current understanding of glucose metabolism, with an emphasis on the transcription factors and their regulators that are involved in the chronic control of glucose homeostasis.
Gluconeogenesis ; Glucose* ; Glycogenolysis ; Glycolysis ; Homeostasis ; Liver ; Metabolic Networks and Pathways ; Metabolism* ; Negotiating ; Protein Processing, Post-Translational ; Transcription Factors

PURPOSE: To elucidate the molecular basis of muscle atrophy in cellular adaptation point of view, gene expression profiling in rat muscle atrophy model was performed. The functions changed by muscle atrophy were analyzed. MATERIAL AND METHODS: Sciatic nerve and femoral nerve were resected in right leg to make muscle atrophy model in rat. The left leg was considered as a compensatory hypertrophy model. The suppression subtractive hybridization (SSH) was done to identify the profile of differential gene expression during muscle atrophy followed by nerve injury in rat. The DNA fragments obtained in SSH were labeled with biotin and used as cDNA tags for isolation of full-length cDNA from cDNA library. Differentially expressed genes were confirmed by reverse dot blot hybridization. RESULTS: Down regulation of genes were much more predominant than up regulation. The profile of down regulated genes were composed of genes coding muscle contractile proteins, enzymes involving carbohydrate metabolism including glycolysis and glycogenolysis, enzymes in oxidative phoshorylation, and proteins related with calcium release. The target genes were isolated by enrichment using cDNA tags from cDNA library for further functional studies. We identified some novel genes related with muscle atrophy by nerve injury. CONCLUSION: During the process of muscle atrophy, genes coding muscle contractile proteins, enzymes in carbohydrate metabolism, enzymes in oxidative phosphorylation, and proteins related with calcium release were down regulated.
Animals ; Atrophy ; Biotin ; Calcium ; Carbohydrate Metabolism ; Chimera ; Clinical Coding ; Contractile Proteins ; DNA ; DNA, Complementary ; Down-Regulation ; Femoral Nerve ; Gene Expression ; Gene Expression Profiling ; Gene Library ; Glycogenolysis ; Glycolysis ; Hypertrophy ; Leg ; Muscle, Skeletal ; Muscles ; Muscular Atrophy ; Oxidative Phosphorylation ; Proteins ; Rats ; Sciatic Nerve ; Up-Regulation

Sucrose is a natural product occurs widely in nature. In living organisms such as plants, sucrose phosphate synthase (SPS) is the key rate-limiting enzyme for sucrose synthesis. SPS catalyzes the synthesis of sucrose-6-phosphate, which is further hydrolyzed by sucrose phosphatase to form sucrose. Researches on SPS in recent decades have been focused on the determination of enzymatic activity of SPS, the identification of the inhibitors and activators of SPS, the covalent modification of SPS, the carbohydrate distribution in plants regulated by SPS, the mechanism for promoting plant growth by SPS, the sweetness of fruit controlled by SPS, and many others. A systematic review of these aspects as well as the crystal structure and catalytic mechanism of SPS are presented.
Carbohydrate Metabolism ; Glucosyltransferases/metabolism* ; Plants/metabolism* ; Sucrose

Despite overall reductions in heart disease prevalence, the risk of developing heart failure has remained 2-fold greater among people with diabetes. Growing evidence has supported that fluctuations in glucose level and uptake contribute to cardiovascular disease (CVD) by modifying proteins, DNA, and gene expression. In the case of glucose, clinical studies have shown that increased dietary sugars for healthy individuals or poor glycemic control in diabetic patients further increased CVD risk. Furthermore, even after decades of maintaining tight glycemic control, susceptibility to disease progression can persist following a period of poor glycemic control through a process termed "glycemic memory." In response to chronically elevated glucose levels, a number of studies have identified molecular targets of the glucose-mediated protein posttranslational modification by the addition of an O-linked N-acetylglucosamine to impair contractility, calcium sensitivity, and mitochondrial protein function. Additionally, elevated glucose contributes to dysfunction in coupling glycolysis to glucose oxidation, pentose phosphate pathway, and polyol pathway. Therefore, in the "sweetened" environment associated with hyperglycemia, there are a number of pathways contributing to increased susceptibly to "breaking" the heart of diabetics. In this review we will discuss the unique contribution of glucose to heart disease and recent advances in defining mechanisms of action.
Calcium ; Cardiomyopathies ; Cardiovascular Diseases ; Diabetic Cardiomyopathies* ; Dietary Sucrose ; Disease Progression ; DNA ; Gene Expression ; Glucose* ; Glycolysis ; Heart ; Heart Diseases ; Heart Failure ; Humans ; Hyperglycemia ; Metabolism ; Mitochondrial Proteins ; Pentose Phosphate Pathway ; Prevalence ; Protein Processing, Post-Translational

A large amount of nicotinamide adenine dinucleotide phosphate (NADPH) is required for fatty acid synthesis and maintenance of the redox state in cancer cells. Malic enzyme 1(ME1)-dependent NADPH production is one of the three pathways that contribute to the formation of the cytosolic NADPH pool. ME1 is generally considered to be overexpressed in cancer cells to meet the high demand for increased de novo fatty acid synthesis. In the present study, we found that glucose induced higher ME1 activity and that repressing ME1 had a profound impact on glucose metabolism of nasopharyngeal carcinoma(NPC) cells. High incorporation of glucose and an enhancement of the pentose phosphate pathway were observed in ME1-repressed cells. However, there were no obvious changes in the other two pathways for glucose metabolism: glycolysis and oxidative phosphorylation. Interestingly, NADPH was decreased under low-glucose condition in ME1-repressed cells relative to wild-type cells, whereas no significant difference was observed under high-glucose condition. ME1-repressed cells had significantly decreased tolerance to low-glucose condition. Moreover, NADPH produced by ME1 was not only important for fatty acid synthesis but also essential for maintenance of the intracellular redox state and the protection of cells from oxidative stress. Furthermore, diminished migration and invasion were observed in ME1-repressed cells due to a reduced level of Snail protein. Collectively, these results suggest an essential role for ME1 in the production of cytosolic NADPH and maintenance of migratory and invasive abilities of NPC cells.
Carcinoma ; Cell Line, Tumor ; Cell Movement ; Cell Survival ; Glucose ; metabolism ; Glycolysis ; Humans ; Malate Dehydrogenase ; metabolism ; NADP ; metabolism ; Nasopharyngeal Neoplasms ; metabolism ; pathology ; Neoplasm Invasiveness ; Oxidation-Reduction ; Oxidative Phosphorylation ; Pentose Phosphate Pathway ; Proto-Oncogene Proteins c-akt ; metabolism

Child ; Humans ; Carbohydrate Metabolism, Inborn Errors ; Microcephaly ; Psychomotor Disorders ; Seizures