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What Is The Glucose Metabolism?

Glucose Metabolism And Hyperglycemia

Glucose Metabolism And Hyperglycemia

From the Department of Geriatrics and Metabolic Diseases, University of Naples SUN, Italy (DG and KE), and the Warwick Medical School, Coventry, United Kingdom (AC) Address correspondence to D Giugliano, Via S Chiara 10/L, 80138 Naples, Italy. E-mail: [email protected] . Search for other works by this author on: From the Department of Geriatrics and Metabolic Diseases, University of Naples SUN, Italy (DG and KE), and the Warwick Medical School, Coventry, United Kingdom (AC) Search for other works by this author on: From the Department of Geriatrics and Metabolic Diseases, University of Naples SUN, Italy (DG and KE), and the Warwick Medical School, Coventry, United Kingdom (AC) Search for other works by this author on: The American Journal of Clinical Nutrition, Volume 87, Issue 1, 1 January 2008, Pages 217S222S, Dario Giugliano, Antonio Ceriello, Katherine Esposito; Glucose metabolism and hyperglycemia, The American Journal of Clinical Nutrition, Volume 87, Issue 1, 1 January 2008, Pages 217S222S, Islet dysfunction and peripheral insulin resistance are both present in type 2 diabetes and are both necessary for the development of hyperglycemia. In both type 1 and type 2 diabetes, large, prospective clinical studies have shown a strong relation between time-averaged mean values of glycemia, measured as glycated hemoglobin (HbA1c), and vascular diabetic complications. These studies are the basis for the American Diabetes Association's current recommended treatment goal that HbA1c should be <7%. The measurement of the HbA1c concentration is considered the gold standard for assessing long-term glycemia; however, it does not reveal any information on the extent or frequency of blood glucose excursions, but provides an overall mean value only. Postprandial hyperglycem Continue reading >>

Physiologic Effects Of Insulin

Physiologic Effects Of Insulin

Stand on a streetcorner and ask people if they know what insulin is, and many will reply, "Doesn't it have something to do with blood sugar?" Indeed, that is correct, but such a response is a bit like saying "Mozart? Wasn't he some kind of a musician?" Insulin is a key player in the control of intermediary metabolism, and the big picture is that it organizes the use of fuels for either storage or oxidation. Through these activities, insulin has profound effects on both carbohydrate and lipid metabolism, and significant influences on protein and mineral metabolism. Consequently, derangements in insulin signalling have widespread and devastating effects on many organs and tissues. The Insulin Receptor and Mechanism of Action Like the receptors for other protein hormones, the receptor for insulin is embedded in the plasma membrane. The insulin receptor is composed of two alpha subunits and two beta subunits linked by disulfide bonds. The alpha chains are entirely extracellular and house insulin binding domains, while the linked beta chains penetrate through the plasma membrane. The insulin receptor is a tyrosine kinase. In other words, it functions as an enzyme that transfers phosphate groups from ATP to tyrosine residues on intracellular target proteins. Binding of insulin to the alpha subunits causes the beta subunits to phosphorylate themselves (autophosphorylation), thus activating the catalytic activity of the receptor. The activated receptor then phosphorylates a number of intracellular proteins, which in turn alters their activity, thereby generating a biological response. Several intracellular proteins have been identified as phosphorylation substrates for the insulin receptor, the best-studied of which is insulin receptor substrate 1 or IRS-1. When IRS-1 is activa Continue reading >>

Sugar For The Brain: The Role Of Glucose In Physiological And Pathological Brain Function

Sugar For The Brain: The Role Of Glucose In Physiological And Pathological Brain Function

Go to: Glucose metabolism: fueling the brain The mammalian brain depends on glucose as its main source of energy. In the adult brain, neurons have the highest energy demand [1], requiring continuous delivery of glucose from blood. In humans, the brain accounts for ~2% of the body weight, but it consumes ~20% of glucose-derived energy making it the main consumer of glucose (~5.6 mg glucose per 100 g human brain tissue per minute [2]). Glucose metabolism provides the fuel for physiological brain function through the generation of ATP, the foundation for neuronal and non-neuronal cellular maintenance, as well as the generation of neurotransmitters. Therefore, tight regulation of glucose metabolism is critical for brain physiology and disturbed glucose metabolism in the brain underlies several diseases affecting both the brain itself as well as the entire organism. Here, we provide a comprehensive overview of the functional implications and recent advances in understanding the fundamental role of glucose metabolism in physiological and pathological brain function. Although brain energy metabolism has been investigated for decades, certain aspects remain controversial, in particular in the field of energy substrate consumption and utilization. It is beyond the scope of this review to resolve these controversies; rather it is our aim to highlight conflicting concepts and results to stimulate discussion in key areas. To this end, we review the bioenergetics of neurotransmission, the cellular composition of a metabolic network, the regulation of cerebral blood flow (CBF), how peripheral glucose metabolism and energy homeostasis are sensed and controlled by the CNS, and the tight regulation of cellular survival through glucose-metabolizing enzymes. Glucose is required to provide Continue reading >>

Liver Glucose Metabolism In Humans

Liver Glucose Metabolism In Humans

Information about normal hepatic glucose metabolism may help to understand pathogenic mechanisms underlying obesity and diabetes mellitus. In addition, liver glucose metabolism is involved in glycosylation reactions and connected with fatty acid metabolism. The liver receives dietary carbohydrates directly from the intestine via the portal vein. Glucokinase phosphorylates glucose to glucose 6-phosphate inside the hepatocyte, ensuring that an adequate flow of glucose enters the cell to be metabolized. Glucose 6-phosphate may proceed to several metabolic pathways. During the post-prandial period, most glucose 6-phosphate is used to synthesize glycogen via the formation of glucose 1-phosphate and UDP–glucose. Minor amounts of UDP–glucose are used to form UDP–glucuronate and UDP–galactose, which are donors of monosaccharide units used in glycosylation. A second pathway of glucose 6-phosphate metabolism is the formation of fructose 6-phosphate, which may either start the hexosamine pathway to produce UDP-N-acetylglucosamine or follow the glycolytic pathway to generate pyruvate and then acetyl-CoA. Acetyl-CoA may enter the tricarboxylic acid (TCA) cycle to be oxidized or may be exported to the cytosol to synthesize fatty acids, when excess glucose is present within the hepatocyte. Finally, glucose 6-phosphate may produce NADPH and ribose 5-phosphate through the pentose phosphate pathway. Glucose metabolism supplies intermediates for glycosylation, a post-translational modification of proteins and lipids that modulates their activity. Congenital deficiency of phosphoglucomutase (PGM)-1 and PGM-3 is associated with impaired glycosylation. In addition to metabolize carbohydrates, the liver produces glucose to be used by other tissues, from glycogen breakdown or from de n Continue reading >>

Glucose Metabolism

Glucose Metabolism

Energy is required for the normal functioning of the organs in the body. Many tissues can also use fat or protein as an energy source but others, such as the brain and red blood cells, can only use glucose. Glucose is stored in the body as glycogen. The liver is an important storage site for glycogen. Glycogen is mobilized and converted to glucose by gluconeogenesis when the blood glucose concentration is low. Glucose may also be produced from non-carbohydrate precursors, such as pyruvate, amino acids and glycerol, by gluconeogenesis. It is gluconeogenesis that maintains blood glucose concentrations, for example during starvation and intense exercise. The endocrine pancreas The pancreas has both endocrine and exocrine functions. The endocrine tissue is grouped together in the islets of Langerhans and consists of four different cell types each with its own function. Alpha cells produce glucagon. Beta cells produce proinsulin. Proinsulin is the inactive form of insulin that is converted to insulin in the circulation. Delta cells produce somatostatin. F or PP cells produce pancreatic polypeptide. Regulation of insulin secretion Insulin secretion is increased by elevated blood glucose concentrations, gastrointestinal hormones and Beta adrenergic stimulation. Insulin secretion is inhibited by catecholamines and somatostatin. The role of insulin and glucagon in glucose metabolism Insulin and glucagon work synergistically to keep blood glucose concentrations normal. Insulin: An elevated blood glucose concentration results in the secretion of insulin: glucose is transported into body cells. The uptake of glucose by liver, kidney and brain cells is by diffusion and does not require insulin. Click on the thumbnail for details of the effect of insulin: Glucagon: The effects of glu Continue reading >>

Glucose Metabolism And Regulation: Beyond Insulin And Glucagon

Glucose Metabolism And Regulation: Beyond Insulin And Glucagon

Insulin and glucagon are potent regulators of glucose metabolism. For decades, we have viewed diabetes from a bi-hormonal perspective of glucose regulation. This perspective is incomplete and inadequate in explaining some of the difficulties that patients and practitioners face when attempting to tightly control blood glucose concentrations. Intensively managing diabetes with insulin is fraught with frustration and risk. Despite our best efforts, glucose fluctuations are unpredictable, and hypoglycemia and weight gain are common. These challenges may be a result of deficiencies or abnormalities in other glucoregulatory hormones. New understanding of the roles of other pancreatic and incretin hormones has led to a multi-hormonal view of glucose homeostasis. HISTORICAL PERSPECTIVE Our understanding of diabetes as a metabolic disease has evolved significantly since the discovery of insulin in the 1920s. Insulin was identified as a potent hormonal regulator of both glucose appearance and disappearance in the circulation. Subsequently, diabetes was viewed as a mono-hormonal disorder characterized by absolute or relative insulin deficiency. Since its discovery, insulin has been the only available pharmacological treatment for patients with type 1 diabetes and a mainstay of therapy for patients with insulin-deficient type 2 diabetes.1–7 The recent discovery of additional hormones with glucoregulatory actions has expanded our understanding of how a variety of different hormones contribute to glucose homeostasis. In the 1950s, glucagon was characterized as a major stimulus of hepatic glucose production. This discovery led to a better understanding of the interplay between insulin and glucagon, thus leading to a bi-hormonal definition of diabetes. Subsequently, the discovery of Continue reading >>

Regulation Of Hepatic Glucose Metabolism In Health And Disease

Regulation Of Hepatic Glucose Metabolism In Health And Disease

Regulation of hepatic glucose metabolism in health and disease Max C. Petersen is an M.D.Ph.D. candidate in the Medical Scientist Training Program at Yale University School of Medicine, New Haven, Connecticut, USA. He completed his Ph.D. in cellular and molecular physiology in the laboratory of Gerald Shulman. His research interests include insulin receptor biology and the pathophysiology of hepatic insulin resistance. Daniel F. Vatner is currently Instructor in Medicine (Endocrinology) at the Yale University School of Medicine, New Haven, Connecticut, USA. He received his M.D. and Ph.D. (biochemistry and molecular biology) degrees at The University of Chicago, Illinois, USA, and completed his medicine residency and a fellowship in endocrinology and metabolism at Yale University. His research interests include the pathophysiology and treatment of lipotoxic insulin resistance and non-alcoholic fatty liver disease. His current focus is on the regulation of lipid fluxes to the liver, with a particular interest in adipose tissue physiology. Gerald I. Shulman is the George R. Cowgill Professor of Medicine (Endocrinology) and Cellular & Molecular Physiology at the Yale University School of Medicine, New Haven, Connecticut, USA. He is also an investigator at the Howard Hughes Medical Institute. He has pioneered the use of magnetic resonance spectroscopy in combination with stable isotopes to study intrahepatic and intramyocellular glucose and lipid metabolism, which has led to several paradigm-shifting insights in our understanding of the pathogenesis of type 2 diabetes mellitus. His ongoing research investigates the cellular and molecular mechanisms by which ectopic lipid accumulation in liver and skeletal muscle promotes liver and muscle insulin resistance and increased rat Continue reading >>

Muscle Physiology - Glucose Metabolism

Muscle Physiology - Glucose Metabolism

Two different pathways are involved in the metabolism of glucose: one anaerobic and one aerobic. The anaerobic process occurs in the cytoplasm and is only moderately efficient. The aerobic cycle takes place in the mitochondria and is results in the greatest release of energy. As the name implies, though, it requires oxygen. Glucose in the bloodstream diffuses into the cytoplasm and is locked there by phosphorylation. A glucose molecule is then rearranged slightly to fructose and phosphorylated again to fructose diphosphate. These steps actually require energy, in the form of two ATPs per glucose. The fructose is then cleaved to yield two glyceraldehyde phosphates (GPs). In the next steps, energy is finally released, in the form of two ATPs and two NADHs , as the GPs are oxidized to phosphoglycerates. One of the key enzymes in this process is glyceraldehyde phosphate dehydrogenase (GPDH), which transfers a hydrogen atom from the GP to NAD to yield the energetic NADH . Due to its key position in the glycolytic pathway, biochemical assays of GPDH are often used to estimate the glycolytic capacity of a muscle cell. Finally, two more ATPs are produced as the phosphoglycerates are oxidized to pyruvate. Pyruvate is the starting molecule for oxidative phosphorylation via the Krebb's or citric acid cycle. In this process, all of the C-C and C-H bonds of the pyruvate will be transferred to oxygen. The pathway can be seen in the figure below. Basically, the pyruvate is oxidized to acetyl coenzyme A, which can then bind with the four carbon oxaloacetate to generate a six carbon citrate. Carbons and hydrogens are gradually cleaved from this citrate until all that remains is the four carbon oxaloacetate we started with. In the process, four NADHs , one FADH and one GTP are generated Continue reading >>

What Is The Process Of Glucose Metabolism? Why Is It Important? - Quora

What Is The Process Of Glucose Metabolism? Why Is It Important? - Quora

What is the process of glucose metabolism? Why is it important? Answered Sep 4, 2016 Author has 373 answers and 203k answer views Glucose is stored in the body as glycogen. The liver is an important storage site for glycogen. Glycogen is mobilized and converted to glucose by gluconeogenesis when the blood glucose concentration is low. Glucose may also be produced from non-carbohydrate precursors, such as pyruvate, amino acids and glycerol, by gluconeogenesis. It is gluconeogenesis that maintains blood glucose concentrations, for example during starvation and intense exercise. To get more effective and useful tips on metabolism - Download free ebook. Answered Jul 21, 2016 Author has 89 answers and 42k answer views Cells inside the human body mostly need glucose for proper functioning. By glucose metabolism, the body technically is able to supply the cells with much-needed fuel. Glucose metabolism is the process which generally converts glucose into energy for cell utilization. This energy mostly is in the form of adenosine triphosphate (ATP). Glycolysis is the term commonly used for the breakdown of glucose into energy for cell use. The body usually derives glucose from carbohydrates. Many foods which are rich in carbohydrates have high starch and sugar content. They mostly include potatoes, pastas, breads, cereals, rice, and candies. After meals, carbohydrate metabolism technically takes place in the digestive tract where they are converted into glucose and absorbed in the blood. As the glucose level in the blood increases, the pancreas, which is part of the endocrine system, usually is stimulated to release the hormone insulin. Continue reading >>

Glucose Metabolism - Metabolism And Hormones - Diapedia, The Living Textbook Of Diabetes

Glucose Metabolism - Metabolism And Hormones - Diapedia, The Living Textbook Of Diabetes

Despite periods of feeding and fasting, in normal individuals plasma glucose remains in a narrow range between 4 and 7 mM reflecting the balance between: (i) the release of glucose into the circulation by either absorption from the intestine or the breakdown of stored glycogen in the liver and (ii) the uptake and metabolism of blood glucose by peripheral tissues [1] . These processes are controlled by a set of metabolic hormones. For decades diabetes had been viewed from a bi-hormonal perspective of glucose regulation involving insulin (discovered in the 1920s; released by pancreatic -cells ) and glucagon (discovered in the 1950s; released by the pancreatic -cells) [2] . In the mid-1970s several gut hormones, the incretins, were identified. One of these, glucagon-like peptide-1 (GLP-1), was recognized as another important contributor to the maintenance of glucose homeostasis. Subsequently the discovery in 1987, of a second pancreatic -cell hormone, amylin, whose role complemented that of insulin, led to the view of glucose homeostasis involving multiple hormones[2]. Amylin, like insulin is found to be deficient in people with diabetes. Hormones produced by adipose tissue also play a critical role in the regulation of energy intake, energy expenditure, and lipid and carbohydrate metabolism. These include leptin, adiponectin, acylation stimulating protein and resistin . Insulin is a key anabolic hormone that is secreted from pancreatic -cells in response to increased blood glucose and amino acids following ingestion of a meal. Insulin, through its action on the insulin receptor decreases blood sugar levels by: (i) increasing glucose uptake in muscle and fat through triggering the translocation of the intracellular glucose transporter GLUT4 to the plasma membrane (see Ins Continue reading >>

Glucose Metabolism - Michael's Naturopathic Programs

Glucose Metabolism - Michael's Naturopathic Programs

Carbohydrate is the name given to a large group of sugars, starches, celluloses, and gums. Carbohydrates are the main source of energy for all body functions and are needed to process other nutrients. Glucose is a major source of energy in human body fluids. When eaten or produced, glucose is taken into the blood from the intestinal tract. Excess glucose in circulation is stored in the liver and muscles as glycogen and converted to glucose and released as needed. Metabolism is the term used to describe the sum of all chemical processes that take place in the body. There are two main types of metabolism; building up, known as anabolism and breaking down, known as catabolism. In anabolism, smaller molecules such as amino acids are converted into larger molecules, such as proteins. In catabolism the opposite is true. Larger molecules, such as glycogen, are broken down to smaller molecules, such as glucose. The hormone insulin serves as the catalyst for the process of catabolism. Insulin is a naturally occurring hormone released by the pancreas in response to increased levels of sugar (glucose) in the blood. Chromium entered into the science of mammalian nutrition in the late 1950s when Schwarz and Mertz reported that rats fed chromium deficient diets exhibited glucose intolerance. Chromium is one of the many trace minerals found in the body. There are two types of minerals that are found throughout the body, trace and macro. These names only indicate the amount of a particular mineral, nothing more. A minerals importance is in no way gauged by its overall content within the body. Some trace minerals, like chromium are essential to the proper functioning of certain enzymatic transactions. The minerals that are found in abundance within the body are referred to as the macro Continue reading >>

Carbohydrate Metabolism

Carbohydrate Metabolism

By the end of this section, you will be able to: Describe the pathway of a pyruvate molecule through the Krebs cycle Explain the transport of electrons through the electron transport chain Describe the process of ATP production through oxidative phosphorylation Carbohydrates are organic molecules composed of carbon, hydrogen, and oxygen atoms. The family of carbohydrates includes both simple and complex sugars. Glucose and fructose are examples of simple sugars, and starch, glycogen, and cellulose are all examples of complex sugars. The complex sugars are also called polysaccharides and are made of multiple monosaccharide molecules. Polysaccharides serve as energy storage (e.g., starch and glycogen) and as structural components (e.g., chitin in insects and cellulose in plants). During digestion, carbohydrates are broken down into simple, soluble sugars that can be transported across the intestinal wall into the circulatory system to be transported throughout the body. Carbohydrate digestion begins in the mouth with the action of salivary amylase on starches and ends with monosaccharides being absorbed across the epithelium of the small intestine. Once the absorbed monosaccharides are transported to the tissues, the process of cellular respiration begins (Figure 1). This section will focus first on glycolysis, a process where the monosaccharide glucose is oxidized, releasing the energy stored in its bonds to produce ATP. Figure 1. Cellular respiration oxidizes glucose molecules through glycolysis, the Krebs cycle, and oxidative phosphorylation to produce ATP. Glucose is the bodys most readily available source of energy. After digestive processes break polysaccharides down into monosaccharides, including glucose, the monosaccharides are transported across the wall of the Continue reading >>

Abnormal Glucose Metabolism In Rheumatoid Arthritis

Abnormal Glucose Metabolism In Rheumatoid Arthritis

BioMed Research International Volume 2017 (2017), Article ID 9670434, 6 pages 1Department of Rheumatology, Jiangxi Provincial People’s Hospital, Nanchang 330006, China 2Department of Critical Care Medicine, The First Affiliated Hospital of Xiamen University, Xiamen 361003, China Academic Editor: Brant R. Burkhardt Copyright © 2017 Hui Pi et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract The incidence of abnormal glucose metabolism in patients with rheumatoid arthritis was considerably higher than the general population. The persistent systemic inflammatory state in rheumatoid arthritis might be associated with the glucose metabolism dysfunction. In this context, insulin resistance, islet β cell apoptosis, inflammatory cytokines, and other aspects which were linked with abnormal glucose metabolism in rheumatoid arthritis were reviewed. This review will be helpful in understanding the abnormal glucose metabolism mechanism in patients with rheumatoid arthritis and might be conducive to finding an effective treatment. 1. Introduction Rheumatoid arthritis (RA) is a systemic autoimmune disease characterized by chronic, symmetry, and destructive poly-articular synovitis. Although its pathogenesis remains unclear, it has shown that inflammation induced by abnormal immune response plays a crucial role in the development of RA. Recent studies show that RA patients with diabetes mellitus (DM) prevalence rate was about 15% to 19%, which was significantly higher than the prevalence rate of 4% to 8% of global middle-aged population DM [1, 2]. In a study, which consists of 48,718 cases of RA patients Continue reading >>

Glucose Metabolism - An Overview | Sciencedirect Topics

Glucose Metabolism - An Overview | Sciencedirect Topics

Satish C. Kalhan, in Fetal and Neonatal Physiology (Fifth Edition) , 2017 Glucose metabolism has been studied extensively in the fetus and newborn, both in animal models and in humans, and several reviews have been published. Our ability to study glucose metabolism has improved significantly because of the availability of (1) the chronic fetal preparation in large animals, in which fetal blood sampling and physiologic monitoring can be done without causing major changes in the state of the fetus; (2) stable, nonradioactive isotopic tracers; and (3) molecular biology techniques and transgenic animals. In this chapter, glucose metabolism in the fetus and newborn is discussed, and recent developments are emphasized. Throughout the chapter, emphasis is placed on the available data in humans, supplemented when necessary with animal data. Wilfred Druml, in Nutritional Management of Renal Disease , 2013 Glucose metabolism in AKI again is affected both by unspecific mechanisms mediated by the acute disease state and specific effects of acute uremia. A major finding is insulin resistance [39]. Plasma insulin concentrations are elevated, maximal insulin-stimulated glucose uptake by skeletal muscle is decreased and muscular glycogen synthesis is impaired [40]. A second feature of glucose metabolism in AKI is accelerated hepatic gluconeogenesis mainly from conversion of amino acids released during protein catabolism [20]. Hepatic extraction of amino acids and their conversion to glucose and urea production are all increased in AKI. As discussed earlier, in contrast to the non-uremic state and CKD, hepatic gluconeogenesis cannot be suppressed completely by exogenous glucose infusions in AKI. Metabolic acidosis also affects glucose metabolism in AKI by further deteriorating glucose Continue reading >>

Glucose Metabolism And Hyperglycemia.

Glucose Metabolism And Hyperglycemia.

Department of Geriatrics and Metabolic Diseases, University of Naples SUN, Italy. [email protected] Islet dysfunction and peripheral insulin resistance are both present in type 2 diabetes and are both necessary for the development of hyperglycemia. In both type 1 and type 2 diabetes, large, prospective clinical studies have shown a strong relation between time-averaged mean values of glycemia, measured as glycated hemoglobin (HbA1c), and vascular diabetic complications. These studies are the basis for the American Diabetes Association's current recommended treatment goal that HbA1c should be <7%. The measurement of the HbA1c concentration is considered the gold standard for assessing long-term glycemia; however, it does not reveal any information on the extent or frequency of blood glucose excursions, but provides an overall mean value only. Postprandial hyperglycemia occurs frequently in patients with diabetes receiving active treatment and can occur even when metabolic control is apparently good. Interventional studies indicate that reducing postmeal glucose excursions is as important as controlling fasting plasma glucose in persons with diabetes and impaired glucose tolerance. Evidence exists for a causal relation between postmeal glucose increases and microvascular and macrovascular outcomes; therefore, it is not surprising that treatment with different compounds that have specific effects on postprandial glucose regulation is accompanied by a significant improvement of many pathways supposed to be involved in diabetic complications, including oxidative stress, endothelial dysfunction, inflammation, and nuclear factor-kappaB activation. The goal of therapy should be to achieve glycemic status as near to normal as safely possible in all 3 components of glyce Continue reading >>

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