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Introduction to Metabolism ط Concept of metabolism, catabolism ط Anabolic and catabolic pathways ط Important consideration for metabolism of carbohydrates, Protein and Lipid ط Overview of metabolic pathways, energetic and regulation D4 268-269, 362-363,446-447
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Introduction 1. Metabolism: intracellular biochemical reaction involve synthesis, conversion, transport & breakdown of various compounds. 2. Anabolism (-genesis): synthesis reactions in metabolism. 3. Catabolism (-lysis): breakdown of metabolites or oxidation: stored in the form of ATP ATP ENERGY ADP + Pi ENERGY AMP + Pi a) Energy produced from high energy compound: e.g. ATP, GTP, UTP -ATP to ADP = 13000 kcal ADP to AMP = 1200 kcal AMP to A = 3000 kcal b) Substrate level phosphorylation: S-P + ADP S + ATP c) Oxidation phosphorylation: -NADH + H 3 ATP -FADH2 2 ATP
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Carbohydrate Metabolism 1. fig7.1: GLYCOGEN (glucose storage) GLUCOSE PYRUVATE …..fig7.1: 2. Defect in Glc metab causes OBESITY & DIABETES: Atherosclerosis, hypertension, kidney disease, blindness
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Lipid Metabolism 1. FA lipid molecules (nonpolar/hydrophobic) 2. fig9.1:TG (FA storage) FA FA / albumine,fig9.1 TG/LP, KB FA ACoA ….. 3. Lipid functions: a) Oxidation of FA ENERGY b) Hydrophobic Structure, FA bound to: -carbohydrates (Glycolipids) -organic phosphate (phospholipids) c) Surface active Properties: -maintenance of lung alveolar integrity -solubolization of nonpolar substances in body fluid -steroid hormones & prostaglandins in metabolic control 4. Deficiencies cause: obesity, diabetes, ketoacidosis & abnormal lipid transport Refsum's Disease & familiar hypercholesterolemia
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Amino Acids Metabolism 1. fig11.1: H2 BACT/PLANT/LIGHT NH3 (ammonia) INCORPORATED AA/Prt (Diet) excretion of NH3 involve sythesis & degradation: Glu, Gln, asp, asn, ala, arg 2. T11.1: -Essential: from diet -Nonessential: de novo biosynthesis 3. T7.2:-Glucogenic: carbon source for Glc synthesis, to Pyr, 3PG, a-KG, OA, Fum, SCoA -Ketogenic: cannot function as carbon source, to ACoA or acetoacetate 4. fig11.2:fig11.2 carbon enters in 7 points a) nonessential b) essential
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Digestion and absorption of carbohydrates ط Digestion and absorption of carbohydrates ط Transport of Monosaccharides ط glucose transporters ط Insulin effect on different transporter ط Lactose intolerance D4 1073-7
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Carbohydrates Digestion 5. Polysaccharides (Branched 100,000 glc mol): α-1, 4-glucosidic bond (amylose) α-1, 6-glucosidic bond (amylopectin) a) Starch (plant); α-1, 4-bond:α-1, 6-bond (ratio 20:1) b) Glycogen (animal); more branches 6. Poly- AMYLASE (salivary & pancreatic) Di- (maltose) MALTASE Mono …..figfig 7. poly- or oligo- (e.g. beans) or di- (e.g. young mushrooms) BACT. (lower ileum) ….. figfig this will cause anaerobic hydrolysis è gases è diarrhea
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Monosaccharide Absorption 1. Intest Luman; Mono- transported by SGLT1: Na+-dependent active transport specific for Glc, Gal by Na+-independent facilitative diffusion: -GLUT5 for Fru -GLUT for all mono 2. Mono transporters or glc trans (GLUT1, 3, 4 ) …… TableTable 3. Insulin Effect on transporters: a) INS-insensitive glc transport system, GLUT2 (liver): Rapid glc uptake & release b) INS-sensitive glc transport system, GLUT5 (muscle/AT): insulin-stimulated glc uptake
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Table: Monosaccharides Transporters FunctionLocation Facilitated-diffusion Transporters Glucose uptakeBrain, Kidney, RBCsGLUT 1 Rapid glucose uptake & releaseLiver, S. intestine, KidneyGLUT 2 Glucose uptakeBrain, KidneyGLUT 3 Insulin-stimulated glucose uptakeMuscle, Adipose tissueGLUT 4 Fructose absorptionS. intestineGLUT 5 Active Na + -dependent Transporter Glucose & galactose absorption & transport S. intestine, KidneySGLT 1 Cytochalasin N is an inhibitor of GLUT 2 Pholorizin is an inhibitor of SGLT 1
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Intestinal Disaccharide Deficiencies: cc26.4 a) In 1 enzyme or more b) Reasons: genetic, age, injury c) Most common is LACTOSE deficiency (milk, lactose intolerance) d) Lower ileum Bact. fermentation causes gas & osmosis lead to diarrhoea e) Yogurt contain partially hydrolyzed lactose f) The enzyme lactase is commercially available
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