DOCSLIB.ORG

Carbohydrate Metabolism and Biological Oxidation Table of Contents

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text

Load more

Carbohydrate Metabolism and Biological Oxidation Table of Contents 1. Digestion and Absorption of Carbohydrates 2. Hormonal Control of Carbohydrate Metabolism 3.Glycogen Synthesis and Degradation 24.4 Gluconeogenesis 24.5 The Pentose Phosphate Pathway 24.6 Glycolysis 24.7 Terminology for Glucose Metabolic Pathways 24.8 The Citric Acid Cycle 24.9 The Electron Transport Chain 24.10 Oxidative Phosphorylation 11. ATP Production for the Complete Oxidation of Glucose 12. Importance of ATP 13. Non-ETC Oxygen-Consuming Reactions 14. B-Vitamins and Carbohydrate Metabolism Copyright © Cengage Learning. All rights reserved 2 Digestion and Absorption of Carbohydrates Copyright © Cengage Learning. All rights reserved 3 Digestion and Absorption of Carbohydrates • Carbohydrate digestion: Begins in the mouth – Salivary enzyme “α-amylase” catalyzes the hydrolysis of α- glycosidic linkages of starch and glycogen to produce smaller polysaccharides and disaccharide – maltose – Only a small amount of carbohydrate digestion occurs in the mouth because food is swallowed so quickly into the stomach • In stomach very little carbohydrate is digested: – No carbohydrate digestion enzymes present in stomach – Salivary amylase gets inactivated because of stomach acidity Copyright © Cengage Learning. All rights reserved 4 Digestion and Absorption of Carbohydrates • The primary site for the carbohydrate digestion is within the small intestine – Pancreatic α-amylase breaks down polysaccharide chains into disaccharide – maltose • The final step in carbohydrate digestion occurs on the outer membranes of intestinal mucosal cells – Maltase – hydrolyses maltose to glucose – Sucrase – hydrolyses sucrose to glucose and fructose – Lactase – hydrolyses lactose to glucose and galactose • Glucose, galactose, and fructose are absorbed into the bloodstream through the intestinal wall. • Galactose and Fructose are converted to products of glucose metabolism in the liver. Copyright © Cengage Learning. All rights reserved 5 Section 24.1 Digestion and Absorption of Carbohydrates • Following absorption the monosaccharides are carried by the portal vein to the liver where galactose and fructose are enzymatically converted to glucose intermediates that enter into the glycolysis pathway • The glucose may then pass into the general circulatory system to be transported to the tissues or converted to glycogen reserve in the liver. • The glucose in the tissues may be a) oxidized to CO2 and H2O (ATP) b) converted to fat c) converted to muscle glycogen Copyright © Cengage Learning. All rights reserved 6 Metabolism • Blood-sugar level: – the proper functions of the body are dependent on precise control of the glucose concentration in the blood. – the normal fasting level of glucose in the blood is 70-90 mg/100 ml. • Abnormal conditions: • A. hypoglycemia – condition resulting from a lower than the normal blood-sugar level (below 70 mg/100 ml) – extreme hypoglycemia, usually due to the presence of excessive amounts of insulin, is characterized by general weakness, trembling, drowsiness, headache, profuse perspiration, rapid heart beat, lowered blood pressure and possible loss ofconsciousness. – Loss of consciousness is most likely due to the lack of glucose in the brain tissue, which is dependent upon this sugar for its energy. • B. hyperglycemia – higher than the normal level (above 120 mg/100 mL); when the pancreas does notsecrete enough insulin – may temporarily exist as a result of eating a meal rich in carbohydrates. – extreme hyperglycemia, the renal threshold (160-170 mg/100 mL) is reached and excess glucose is excreted in the urine Copyright © Cengage Learning. All rights reserved 7 Hormonal Control of Carbohydrate Metabolism • Besides enzyme inhibition, carbohydrate metabolism may be regulated by hormones • Three major hormones control carbohydrate metabolism: – Insulin ; Glucagon ; Epinephrine • Insulin • 51 amino acid polypeptide secreted by the pancreas • Promotes utilization of glucose by cells • The release of insulin is triggered by high blood-glucose levels • Its function is to lower blood glucose levels by enhancing the formation of glycogen from glucose (glycogen synthesis) • The mechanism for insulin action involves insulin binding to proteins receptors on the outer surfaces of cells which facilitates entry of the glucose into the cells Copyright © Cengage Learning. All rights reserved 8 Hormonal Control of Carbohydrate Metabolism Glucagon • 29 amino acid peptide hormone produced in the pancreas • Released when blood glucose levels are low • Principal function is to increase blood-glucose concentration by speeding up the conversion of glycogen to glucose (glycogenolysis) in the liver • Glucagon elicits the opposite effects of insulin Epinephrine (also called adrenaline) • Released by the adrenal glands in response to anger, fear, orexcitement • Function is similar to glucagon, i.e., stimulates glycogenolysis • Primary target of epinephrine is muscle cells • Promotes energy generation for quick action Copyright © Cengage Learning. All rights reserved 9 Metabolism • There are six major metabolic pathways of glucose: 1) Glycogenesis 2) Glycogenolysis 3) Gluconeogenesis 4) Hexose monophosphate shunt 5) Glycolysis 6) Citric Acid Cycle Copyright © Cengage Learning. All rights reserved 10 Glycogen Synthesis and Degradation Glycogenesis and Glycogenolysis • Involved in the regulation of blood glucose concentration • When the dietary intake of glucose exceeds immediate needs, humans and other animals can convert the excess to glycogen, which is stored in either the liver or muscle tissue. • Glycogenesis is the pathway that converts glucose into glycogen. • When there’s need for additional blood glucose, glycogen is hydrolyzed and released into the bloodstream. • Glycogenolysis is the pathway that hydrolyzes glycogen to glucose. Copyright © Cengage Learning. All rights reserved 11 Gluconeogenesis • Metabolic pathway by which glucose is synthesized from non- carbohydrate sources: – The process is not exact opposite of glycolysis • Glycogen stores in muscle and liver tissue are depleted with in 12-18 hours from fasting or in even less time from heavy work or strenuous physical activity • Without gluconeogenesis, the brain, which is dependent on glucose as a fuel would have problems functioning if food intake were restricted for even one day • Gluconeogenesis helps to maintain normal blood-glucose levels in times of inadequate dietary carbohydrate intake • About 90% of gluconeogenesis takes place in the liver • Non-carbohydrate starting materials for gluconeogenesis: – Pyruvate – Lactate (from muscles and from red blood cells) – Glycerol (from triacylglycerol hydrolysis) – Certain amino acids (from dietary protein hydrolysis or from muscle protein during starvation) Copyright © Cengage Learning. All rights reserved 12 The Pentose Phosphate Pathway Hexose monophosphate shunt • Initial reactant of the pathway is glucose-6- phosphate • Also termed phosphogluconate pathway, because 6–phosphogluconate is one of the intermediates • A third name is pentose phosphate pathway, because ribose-5-phosphate is one of its products • The main purposes of the HMP shunt are the following: – to produce ribose-5-P for nucleotide synthesis – to produce NADPH from NADP+ for fatty acid and steroid biosynthesis and for maintaining reduced glutathione (GSH) inside erythrocytes – to interconvert pentoses and hexoses Copyright © Cengage Learning. All rights reserved 13 Glycolysis • A series of reactions in the cytoplasm which converts glucose (C6) to two molecules of pyruvate (a C3 carboxylate), and ATP and NADH are produced. • Also called Embden-Meyerhof pathway, after the scientist who elucidated the pathway • an anaerobic process; each step takes place without O2; one of its advantages, the body can obtain energy from glycolysis quickly, without waiting for a supply of O2 to be carried to the cells. • occurs in cells lacking mitochondria, e.g., erythrocytes and in certain skeletal muscle cells during intense muscle activity Copyright © Cengage Learning. All rights reserved 14 Glycolysis • Step 1: Formation of glucose-6-phosphate: – Endothermic reaction catalyzed by hexokinase – Energy needed is derived from ATP hydrolysis • Step 2: Formation of Fructose-6-phosphate: – Enzyme: Phosphoglucoisomerase • Step 3: Formation of Fructose 1,6-bisphosphate: – Enzyme: phosphofructokinase • Step 4: Formation of Triose Phosphates: – C6 species is split into two C3 species – Enzyme : Aldolase • Step 5: Isomerization of Triose Phosphates – DHAP is isomerized to glyceraldehyde 3- phosphate – Enzyme: Triosephosphate isomerase • Step 6: Formation of 1,3-bisphosphoglycerate – Glyceraldehyde 3-phosphate is oxidized and phosphorylated – Enzyme: Glyceraldehyde-3-phosphate dehydrogenase Copyright © Cengage Learning. All rights reserved 15 Glycolysis • Step 7: Formation of 3-bisphosphoglycerate – It is an ATP producing step – Enzyme: phosphoglycerokinase • Step 8: Formation of 2-phosphoglycerate – Isomerization of 3-phosphoglycerate to 2-phosphoglycerate – Enzyme: phosphoglyceromutase • Step 9: Formation of Phosphoenolpyruvate: – Enzyme: Enolase • Step 10: Formation of Pyruvate: – High energy phosphate is transferred from phosphoenolpyruvate to ADP molecule to produce ATP and pyruvate – Enzyme: Pyruvate kinase • At this point of carbohydrate metabolism there are at least 2 directions that the product pyruvate may take. • The direction depends primarily upon the availability of oxygen in the cell: Copyright © Cengage Learning.
Recommended publications
  • • Glycolysis • Gluconeogenesis • Glycogen Synthesis

    • Glycolysis • Gluconeogenesis • Glycogen Synthesis

    Carbohydrate Metabolism! Wichit Suthammarak – Department of Biochemistry, Faculty of Medicine Siriraj Hospital – Aug 1st and 4th, 2014! • Glycolysis • Gluconeogenesis • Glycogen synthesis • Glycogenolysis • Pentose phosphate pathway • Metabolism of other hexoses Carbohydrate Digestion! Digestive enzymes! Polysaccharides/complex carbohydrates Salivary glands Amylase Pancreas Oligosaccharides/dextrins Dextrinase Membrane-bound Microvilli Brush border Maltose Sucrose Lactose Maltase Sucrase Lactase ‘Disaccharidase’ 2 glucose 1 glucose 1 glucose 1 fructose 1 galactose Lactose Intolerance! Cause & Pathophysiology! Normal lactose digestion Lactose intolerance Lactose Lactose Lactose Glucose Small Intestine Lactase lactase X Galactose Bacteria 1 glucose Large Fermentation 1 galactose Intestine gases, organic acid, Normal stools osmotically Lactase deficiency! active molecules • Primary lactase deficiency: อาการ! genetic defect, การสราง lactase ลด ลงเมออายมากขน, พบมากทสด! ปวดทอง, ถายเหลว, คลนไสอาเจยนภาย • Secondary lactase deficiency: หลงจากรบประทานอาหารทม lactose acquired/transient เชน small bowel เปนปรมาณมาก เชนนม! injury, gastroenteritis, inflammatory bowel disease! Absorption of Hexoses! Site: duodenum! Intestinal lumen Enterocytes Membrane Transporter! Blood SGLT1: sodium-glucose transporter Na+" Na+" •! Presents at the apical membrane ! of enterocytes! SGLT1 Glucose" Glucose" •! Co-transports Na+ and glucose/! Galactose" Galactose" galactose! GLUT2 Fructose" Fructose" GLUT5 GLUT5 •! Transports fructose from the ! intestinal lumen into enterocytes!
  • Fatty Acid Biosynthesis

    Fatty Acid Biosynthesis

    BI/CH 422/622 ANABOLISM OUTLINE: Photosynthesis Carbon Assimilation – Calvin Cycle Carbohydrate Biosynthesis in Animals Gluconeogenesis Glycogen Synthesis Pentose-Phosphate Pathway Regulation of Carbohydrate Metabolism Anaplerotic reactions Biosynthesis of Fatty Acids and Lipids Fatty Acids contrasts Diversification of fatty acids location & transport Eicosanoids Synthesis Prostaglandins and Thromboxane acetyl-CoA carboxylase Triacylglycerides fatty acid synthase ACP priming Membrane lipids 4 steps Glycerophospholipids Control of fatty acid metabolism Sphingolipids Isoprene lipids: Cholesterol ANABOLISM II: Biosynthesis of Fatty Acids & Lipids 1 ANABOLISM II: Biosynthesis of Fatty Acids & Lipids 1. Biosynthesis of fatty acids 2. Regulation of fatty acid degradation and synthesis 3. Assembly of fatty acids into triacylglycerol and phospholipids 4. Metabolism of isoprenes a. Ketone bodies and Isoprene biosynthesis b. Isoprene polymerization i. Cholesterol ii. Steroids & other molecules iii. Regulation iv. Role of cholesterol in human disease ANABOLISM II: Biosynthesis of Fatty Acids & Lipids Lipid Fat Biosynthesis Catabolism Fatty Acid Fatty Acid Degradation Synthesis Ketone body Isoprene Utilization Biosynthesis 2 Catabolism Fatty Acid Biosynthesis Anabolism • Contrast with Sugars – Lipids have have hydro-carbons not carbo-hydrates – more reduced=more energy – Long-term storage vs short-term storage – Lipids are essential for structure in ALL organisms: membrane phospholipids • Catabolism of fatty acids –produces acetyl-CoA –produces reducing
  • Carbohydrate Metabolism I & II Central Aspects of Macronutrient

    Carbohydrate Metabolism I & II Central Aspects of Macronutrient

    Carbohydrate Metabolism I & II - General concepts of glucose metabolism - - Glycolysis - -TCA - FScN4621W Xiaoli Chen, PhD Food Science and Nutrition University of Minnesota 1 Central Aspects of Macronutrient Metabolism Macronutrients (carbohydrate, lipid, protein) Catabolic metabolism Oxidation Metabolites (smaller molecules) Anabolic metabolism Energy (ATP) Synthesis of cellular components or energy stores Chemical Reactions Cellular Activities 2 Central Aspects of Macronutrient Metabolism High-energy compounds ◦ ATP (adenosine triphosphate) ◦ NADPH (reduced nicotinamide adenine dinucleotide phosphate) ◦ NADH (reduced nicotinamide adenine dinucleotide) ◦ FADH2 (reduced flavin adenine dinucleotide) Oxidation of macronutrients NADH NADPH FADH2 ATP and NADPH are required ATP for anabolic metabolism 3 1 Unit I General Concepts of Glucose Metabolism Metabolic pathways of glucose Glucose homeostasis Glucose transport in tissues Glucose metabolism in specific tissues 4 Overview Digestion, Absorption and Transport of Carbs ◦ Final products of digestion: ________, ________, and ________ Cellular fuels ◦ Glucose, fatty acids, ketone bodies, amino acids, other gluoconeogenic precursors (glycerol, lactate, propionate) Glucose: primary metabolic fuel in humans ◦ Provide 32% to 70% of the energy in diet of American population All tissues are able to use glucose as energy fuels ◦ Glucose has different metabolic fate in different tissues Physiological states determine glucose metabolic fate ◦ Fed/fasted – glucose is metabolized through distinct
  • Regulation of Muscle Glycogen Metabolism During Exercise: Implications for Endurance Performance and Training Adaptations

    Regulation of Muscle Glycogen Metabolism During Exercise: Implications for Endurance Performance and Training Adaptations

    nutrients Review Regulation of Muscle Glycogen Metabolism during Exercise: Implications for Endurance Performance and Training Adaptations Mark A. Hearris, Kelly M. Hammond, J. Marc Fell and James P. Morton * Research Institute for Sport & Exercise Sciences, Liverpool John Moores University, Liverpool L3 3AF, UK; [email protected] (M.A.H.); [email protected] (K.M.H.); [email protected] (J.M.F.) * Correspondence: [email protected]; Tel.: +44-151-904-6233 Received: 9 January 2018; Accepted: 27 February 2018; Published: 2 March 2018 Abstract: Since the introduction of the muscle biopsy technique in the late 1960s, our understanding of the regulation of muscle glycogen storage and metabolism has advanced considerably. Muscle glycogenolysis and rates of carbohydrate (CHO) oxidation are affected by factors such as exercise intensity, duration, training status and substrate availability. Such changes to the global exercise stimulus exert regulatory effects on key enzymes and transport proteins via both hormonal control and local allosteric regulation. Given the well-documented effects of high CHO availability on promoting exercise performance, elite endurance athletes are typically advised to ensure high CHO availability before, during and after high-intensity training sessions or competition. Nonetheless, in recognition that the glycogen granule is more than a simple fuel store, it is now also accepted that glycogen is a potent regulator of the molecular cell signaling pathways that regulate the oxidative phenotype. Accordingly, the concept of deliberately training with low CHO availability has now gained increased popularity amongst athletic circles. In this review, we present an overview of the regulatory control of CHO metabolism during exercise (with a specific emphasis on muscle glycogen utilization) in order to discuss the effects of both high and low CHO availability on modulating exercise performance and training adaptations, respectively.
  • Energetics of Carbohydrate Metabolism Cellular Respiration Can

    Energetics of Carbohydrate Metabolism Cellular Respiration Can

    Energetics of carbohydrate metabolism Cellular respiration can take place either in the presence or absence of oxygen leaving separate end products respectively. Metabolism of glucose leads to its breakdown to pyruvate. This pyruvate can have one of the following three fates: 1. Breaks down to lactic acid in the presence of enzyme lactate dehydrogenase in vigorously contracting skeletal muscles, in certain micro-organisms etc. (called lactic acid fermentation) (Anaerobic Respiration) 2. Breaks down to ethanol and carbon dioxide in some plant tissues, invertebrates and microorganisms (e.g. yeast) (called alcoholic fermentation) (Anaerobic Respiration) 3. Enters aerobic respiration in Kreb’s Cycle to form carbon dioxide and water. (Aerobic Respiration) These glucose molecules can be either stored as starch or glycogen in the body. When excessive energy is demanded by the body, this reserve is broken down to produce energy aerobically or anaerobically. Aerobic respiration takes place in three steps: 1. Glycolysis or Embden-Meyerhof pathway: All glycolysis reactions take place in the cytosol as all the enzymes required for the pathway are present here. In glycolysis one glucose molecule is converted to two pyruvate molecules with the release of energy in the form of ATP and NADH. This pathway is divided into two phases the preparatory phase and the pay-off phase. 2. Kreb’s Cycle or Citric Acid Cylce or Tricarboxylic Acid Cycle: The pyruvate formed in glycolysis then gets converted to acetyl CoA in the mitochondria. In the mitochondria enzymatic reactions occur known as Kreb’s Cycle to breakdown the acetyl CoA into CO2 and H2O with the release of energy in the form of ATP, NADH and FADH2.
  • Carbohydrate Metabolism-1.Pptx

    Carbohydrate Metabolism-1.Pptx

    Carbohydrate Metabolism Assist.Prof.Dr. Filiz BAKAR ATEŞ Introduction to Metabolism ò In cells, enzymatic reactions are organized into multistep sequences called pathways, ò Glycolysis, gluconeogeesis, etc. ò In a pathway: the product of one reaction serves as the substrate of the subsequent reaction. Introduction to Metabolism ò Metabolism: the sum of all the chemical changes occurring in a cell, a tissue, or the body. ò Most pathways can be classified as either catabolic (degradative) or anabolic (synthetic). ò Catabolic reactions break down complex molecules, such as proteins, polysaccharides, and lipids, to a few simple molecules, for example, CO2, NH3 (ammonia), and water. ò Anabolic pathways form complex end products from simple precursors, for example, the synthesis of the polysaccharide, glycogen, from glucose Metabolic Map ò Each metabolic pathway is composed of multienzyme sequences, and each enzyme, in turn, may exhibit important catalytic or regulatory features. Catabolic Pathways ò Catabolic reactions serve to capture chemical energy in the form of adenosine triphosphate (ATP) from the degradation of energy-rich fuel molecules. ò Catabolism also allows molecules in the diet (or nutrient molecules stored in cells) to be converted into building blocks needed for the synthesis of complex molecules. Anabolic pathways ò Anabolic reactions combine small molecules, such as amino acids, to form complex molecules, such as proteins ò Require energy (endergonic), which is generally provided by the breakdown of ATP to adenosine diphosphate (ADP) and inorganic phosphate (Pi). ò Anabolic reactions often involve chemical reductions in which the reducing power is most frequently provided by the electron donor NADPH. ò Catabolism is a convergent process—that is, a wide variety of molecules are transformed into a few common end products.
  • Metabolic Fate of Glucose Metabolic Fate of Fatty Acids

    Metabolic Fate of Glucose Metabolic Fate of Fatty Acids

    CHEM464/Medh, J.D. Integration of Metabolism Metabolic Fate of Glucose • Each class of biomolecule has alternative fates depending on the metabolic state of the body. • Glucose: The intracellular form of glucose is glucose-6- phosphate. • Only liver cells have the enzyme glucose-6-phosphatase that dephosphorylates G-6-P and releases glucose into the blood for use by other tissues • G-6-P can be oxidized for energy in the form of ATP and NADH • G-6-P can be converted to acetyl CoA and then fat. • Excess G-6-P is stored away as glycogen. • G-6-P can be shunted into the pentose phosphate pathway to generate NADPH and ribose-5-phosphate. Metabolic Fate of Fatty Acids • Fatty acids are oxidized to acetyl CoA for energy production in the form of NADH. • Fatty acids can be converted to ketone bodies. KB can be used as fuel in extrahepatic tissues. • Palmityl CoA is a precursor of mono- and poly- unsaturated fatty acids. • Fatty acids are used for the biosynthesis of bioactive molecules such as arachidonic acid and eicosanoids. • Cholesterol, steroids and steroid hormones are all derived from fatty acids. • Excess fatty acids are stored away as triglycerides in adipose tissue. 1 CHEM464/Medh, J.D. Integration of Metabolism Metabolic Fate of Amino Acids • Amino acids are used for the synthesis of enzymes, transporters and other physiologically significant proteins. • Amino acid N is required for synthesis of the cell’s genetic information (synthesis of nitrogenous bases). • Several biologically active molecules such as neuro- transmitters, porphyrins etc. • Amino acids are precursors of several hormones (peptide hormones like insulin and glucagon and Amine hormones such as catecholamines).
  • Lipid and Carbohydrate Metabolism in Caenorhabditis Elegans

    Lipid and Carbohydrate Metabolism in Caenorhabditis Elegans

    | WORMBOOK METABOLISM, PHYSIOLOGY, AND AGING Lipid and Carbohydrate Metabolism in Caenorhabditis elegans Jennifer L. Watts*,1 and Michael Ristow† *School of Molecular Biosciences and Center for Reproductive Biology, Washington State University, Pullman, Washington 99164 and †Energy Metabolism Laboratory, Institute of Translational Medicine, Department of Health Sciences and Technology, Swiss Federal Institute of Technology Zurich, 8603 Schwerzenbach-Zurich, Switzerland ORCID ID: 0000-0003-4349-0639 (J.L.W.) ABSTRACT Lipid and carbohydrate metabolism are highly conserved processes that affect nearly all aspects of organismal biology. Caenorhabditis elegans eat bacteria, which consist of lipids, carbohydrates, and proteins that are broken down during digestion into fatty acids, simple sugars, and amino acid precursors. With these nutrients, C. elegans synthesizes a wide range of metabolites that are required for development and behavior. In this review, we outline lipid and carbohydrate structures as well as biosynthesis and breakdown pathways that have been characterized in C. elegans. We bring attention to functional studies using mutant strains that reveal physiological roles for specific lipids and carbohydrates during development, aging, and adaptation to changing environmental conditions. KEYWORDS Caenorhabditis elegans; ascarosides; glucose; fatty acids; phospholipids; sphingolipids; triacylglycerols; cholesterol; maradolipids; WormBook TABLE OF CONTENTS Abstract 413 Fatty Acids 415 Characteristics of C. elegans fatty acids 415 Methods
  • Ch22: Carbohydrate Metabolism Catabolism Overview Diges�On of Carbohydrates Villi of Small Intes�Ne [Handout] Catabolism Flow Chart

    Ch22: Carbohydrate Metabolism Catabolism Overview DigesOn of Carbohydrates Villi of Small IntesNe [Handout] Catabolism Flow Chart

    Chem 30B Ch22: Carbohydrate Metabolism Catabolism Overview Diges;on of Carbohydrates Villi of Small Intes;ne [Handout] Catabolism Flow Chart FOOD LIPIDS PROTEINS CARBOHYDRATES Fatty Acids + Glycerols Glucose + Amino Acids Other Sugars Pentose Phosphate Amino Acid Fatty Acids Pathway Glycogenesis Catabolism 5-C sugars Glycogen + NAPDH Glucose 6-phosphate β-oxidation Glycolysis 2 NADH + 2 ATP *Glycolysis yields 2 pyruvates, so multiply everything below by 2x! O O Anaerobic - H3C C C O Lactate n NADH Pyruvate Aerobic + n FADH2 (n depends on carbon CO2 NADH length of fatty acid) O Steroids H3C C SCoA Ketone Protein bodies Acetyl-CoA metabolism Citric Acid Cycle 1 ATP 2 CO2 3 NADH, 1 FADH2 O2 Electron Transport Chain & Oxidative H2O Phosphorylation 11 ATP (3 ATP/NADH + 2 ATP/FADH2) [Handout] Glycolysis HO CH 2- 2 Hexokinase O3PO CH2 Fructose 6-phosphate kinase O OH OH Glucose 6-phosphate ATP ADP O OH isomerase 2-O PO CH ATP ADP 3 2 O OH H H OH H OH 1 OH H OH H 3 2 H CH2OH H OH OH H OH H Glucose Glucose 6-phosphate Fructose 6-phophate O H2 2- O3PO C C CH2OH Dihydroxyacetone phosphate 2- OH O3PO CH2 O Aldolase H OH Triose phosphate 5 isomerase H 2- CH2OPO3 4 Glyceraldehyde 3-phosphate OH H dehydrogenase O OH O Fructose 1,6-bisphosphate OH H2 H2 NAD+ NADH/H+ HOPO 2- 2- 3 2-O PO C C C OPO 2- O3PO C C CH 3 3 H H D-Glyceraldehyde 6 1,3-Bisphosphoglycerate 3-phosphate Phosphoglycerate kinase H2O OPO 2– Enolase OPO 2– ADP ATP Phosphoglycerate mutase 3 3 OH O O H2 H O 2- – 2 – O3PO C C C O HO C C C O– H2C C C O H 9 7 8 H 3-Phosphoglycerate 2-Phosphoglycerate Phosphoenolpyruvate Pyruvate kinase ADP ATP O O – H3C C C O 10 Pyruvate Glucose to Acetyl-CoA Glucose and Fatty Acid Catabolism I.
  • JCI96702.Pdf

    JCI96702.Pdf

    Downloaded from http://www.jci.org on February 6, 2018. https://doi.org/10.1172/JCI96702 The Journal of Clinical Investigation REVIEW Fructose metabolism and metabolic disease Sarah A. Hannou,1 Danielle E. Haslam,2 Nicola M. McKeown,2 and Mark A. Herman1 1Division of Endocrinology and Metabolism and Duke Molecular Physiology Institute, Duke University Medical Center, Durham, North Carolina, USA. 2Nutritional Epidemiology Program, Jean Mayer US Department of Agriculture Human Nutrition Research Center on Aging, Tufts University, Boston, Massachusetts, USA. Increased sugar consumption is increasingly considered to be a contributor to the worldwide epidemics of obesity and diabetes and their associated cardiometabolic risks. As a result of its unique metabolic properties, the fructose component of sugar may be particularly harmful. Diets high in fructose can rapidly produce all of the key features of the metabolic syndrome. Here we review the biology of fructose metabolism as well as potential mechanisms by which excessive fructose consumption may contribute to cardiometabolic disease. Introduction recent prospective study showed that daily SSB consumers had a Glucose is the predominant form of circulating sugar in animals, 29% greater increase in visceral adipose tissue volume over 6 years while sucrose, the disaccharide composed of equal portions of glu- compared with nonconsumers (9). A causal association is sup- cose and fructose, is the predominant circulating sugar in plants. ported by evidence that intake of 1 liter of SSB daily for 6 months As plants form the basis of the food chain, herbivores and omni- increased visceral and liver fat, but increases were not observed in vores are highly adapted to use sucrose for energetic and biosyn- those consuming isocaloric semiskim milk, noncaloric diet soda, or thetic needs.
  • CHO Metabolism

    CHO Metabolism

    Handout 5 Carbohydrate Metabolism ANSC/NUTR 601 PHYSIOLOGICAL CHEMISTRY OF LIVESTOCK SPECIES Carbohydrate Metabolism I. Glycolysis A. Pathway Regulation of glycolysis Hexokinase: Activated by glucose. Inhibited by G6P. 6-Phosphofructokinase: Inhibited by ATP, especially in the presence of citrate. Activated by AMP. B. Pyruvate and lactate 1 Handout 5 Carbohydrate Metabolism 2 Handout 5 Carbohydrate Metabolism C. Entry of fructose into glycolysis 1. Fructose – Phosphorylated by fructokinase to fructose-1-phosphate, then split to DHAP and glyceraldehyde. II. Krebs (tricarboxylic acid or citric acid) cycle A. Conversion of pyruvate to acetyl CoA 1. Pyruvate is decarboxylated by pyruvate dehydrogenase at the inner mitochondrial membrane. 2. Coenzyme A is attached by a thioester bond to acetate to form acetyl-CoA B. Conversion of pyruvate to oxaloacetate 1. Pyruvate crosses the inner mitochondrial membrane. 2. Pyruvate is carboxylated to oxaloacetate in the mitochondrial matrix. C. The cycle 1. Oxaloacetate condenses with acetyl-CoA to initiate the TCA cycle. 2. A net of two carbons is lost during one complete cycle. 3. Primary regulation is at isocitrate dehydrogenase. 3 Handout 5 Carbohydrate Metabolism NADH (-) ADP (+) III. Gluconeogenesis A. Essential enzymes 1. Pyruvate carboxylase (converts pyruvate to oxaloacetate) 2. Phosphoenolpyruvate carboxykinase (PEPCK) (converts oxaloacetate to PEP) 3. Fructose 1,6-diphosphatase (converts fructose 1,6-diphosphate to F-6-P). 4. Glucose-6-phosphates (converts G-6-P to free glucose) B. Overall pathway Pyruvate à oxaloacetate à PEP à à Fructose 1,6-diphosphate à F-6-P à G-6-P à Glucose C. Organs responsible for gluconeogenesis 4 Handout 5 Carbohydrate Metabolism A.
  • Intermediary Carbohydrate Metabolism

    Intermediary Carbohydrate Metabolism

    J Clin Pathol: first published as 10.1136/jcp.s1-2.1.66 on 1 January 1969. Downloaded from J. clin. Path., 22, suppl. (Ass. clin. Path.), 2, 66-71 Intermediary carbohydrate metabolism P. J. RANDLE From the Department ofBiochemistry, University of Bristol Current interest in mammalian carbohydrate meta- may act by raising substrate Km or lowering Vmax bolism is largely centred on the operation of or both. They may conform to classical inhibitor metabolic pathways in tissues and whole animals. kinetics (see Dixon and Webb. 1958) or the rela- Recent studies have indicated that the various tionship between degree of inhibition and inhibitor pathways may be controlled by one or two key concentration may be sigmoid (ie, show a threshold). enzymes which function as pacemakers. Trans- Similar considerations may be applied to activators. porting systems in the plasma membrane and also In general it is important to distinguish between in intracellular membranes, such as the mitochon- those inhibitors which influence Vmax alone, Km drial membrane, are of increasing importance in alone, and both Vmax and Km. Where only K. is control and hence in the operation of metabolic altered inhibition may be overcome by compensatory pathways. changes in substrate concentration; this will not be the case when only Vmax is altered. CONTROL IN TISSUES The identification of pacemaker reactions in metabolic pathways has depended upon simul- The majority of enzymes and transporting systems taneous measure-ments of rates of flow and con- in carbohydrate metabolism probably conform to centrations of substrates and products of individual Michaelis-Menten kinetics. The relationship be- reactions in tissues.