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Chapter 4 Carbohydrates

Chapter 4 Carbohydrates. Objectives: Learn the major sources of dietary carbohydrates. What are these digested to and absorbed as? What are the major types of glucose transporters and where are they found? How are these transporters regulated?

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Chapter 4 Carbohydrates

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  1. Chapter 4 Carbohydrates Objectives: • Learn the major sources of dietary carbohydrates. • What are these digested to and absorbed as? • What are the major types of glucose transporters and where are they found? How are these transporters regulated? • Understand how the major carbohydrates are utilized metabolically by your cells • Understand the basic processes involved in glycolysis, glycogenesis, glycogenolysis, gluconeogenesis, and the hexosemonophosphate shunt • Understand how fructose and galactose enter these pathways • Learn how these pathways are regulated by insulin and glucagon • What are the major ways that regulation takes place (mechanisms of regulation)? • Learn how ethanol consumption impacts the metabolic pathways for carbohydrates • Acetaldehyde toxicity • High NADH:NAD+ ratio • Substrate competition • Induced metabolic tolerance • Learn how some diseases are associated with carbohydrate metabolism • Diabetes • Hypoglycemia

  2. Enzymes involved in carbohydrate digestion and metabolism are stereospecific for D sugars Reference molecule Chiral carbon? Anomeric carbon? Fig. 4-2, p. 74

  3. Pentoses? Reducing sugars? Oligosaccharides? Table 4-1, p. 75

  4. Fig. 4-5a, p. 77

  5. r Fig. 4-6, p. 78

  6. Table 4-2, p. 81

  7. Golgi Apparatus Glucose Transport Vesicle-bound transporters Synthesized transporters from ribosomes Translocation Signal? Insulin Insulin receptor Fig. 4-8, p. 82

  8. (a) Glucose (reference food) (b) Low glycemic index (c) Fasting baseline Blood glucose (mg/dL) Hours Glucose meal Fig. 4-9, p. 83

  9. Fig. 4-10, p. 84

  10. Fig. 4-11a, p. 85

  11. Glycogen synthase – active when dephosphorylated, inactive when phosphorylated; insulin vs. glucagon Fig. 4-11b, p. 85

  12. Glycogenolysis – activated by glucagon and epinephrine through action on glycogen phosphorylase (phosphorylase a, phosphorylated – active; phosphorylase b, dephosphorylated - inactive Fig. 4-12, p. 86

  13. Fig. 4-13, p. 87

  14. Fig. 4-14, p. 88

  15. Citrate synthase • Aconitase • Isocitrate dehydrogenase • a ketoglutarate dehydrogenase • Succinyl thiokinase • Succinate dehydrogenase • Fumarase • Malate dehydrogenase Fig. 4-15, p. 91

  16. Fig. 4-16, p. 91

  17. Fig. 4-17, p. 93

  18. Used when nucleic acids are needed Used when NADPH is needed Fig. 4-19, p. 95

  19. Brain, neurons, and RBCs are dependent on glucose as a nutrient. When dietary intake of glucose is decreased and glycogen stores are depleted, we can make new glucose from alternative fuel sources in a process called gluconeogenesis • Fuels used to make new glucose include • amino acids, • lactate, • Glycerol • Organ which most often performs gluconeogenesis is the liver

  20. Irreversible rxn Fig. 4-21, p. 97

  21. Four Mechanisms for Regulating Blood Glucose • Allosteric modulation by compounds within the pathways • Hormonal activation of covalent modification of specific enzymes • Directional shifts in reversible reactions by changes in reactant or product concentrations • Translocation of enzymes within the cell

  22. Citrate synthase • Aconitase • Isocitrate dehydrogenase • a ketoglutarate dehydrogenase • Succinyl thiokinase • Succinate dehydrogenase • Fumarase • Malate dehydrogenase Regulated by NADH/NAD+ Regulated by ATP/ADP Fig. 4-15, p. 91

  23. Fig. 4-22, p. 101

  24. Ethyl Alcohol: Metabolic Impact • Ethyl alcohol most closely resembles a carbohydrate • It has caloric value, and is a common dietary component of alcoholic beverages • Each gram of alcohol yields 7kcal of energy • May account for 10% of total energy intake in moderate consumers • May account for 50% of total energy intake in alcoholics. • Ethanol is absorbed throughout the digestive tract and is transported in the blood. • It is then oxidatively degraded, mostly in the liver, to acetaldehyde and then to acetate. Acetate eventually is converted to acetylcoA • Alcohol dehydrogenase • MEOS or cytochrome P-450 • catalase

  25. ethanol + NAD+ ----> acetaldehyde + NADH Acetaldehyde is toxic reactive with amino groups and may interact with proteins competes for the plasma carrier of pyridoxal (vitamin B6) acetaldehyde + NAD+ ----> acetic acid + NADH Acetic acid can lead to acidosis Because the two reactions require NAD+, NADH can build up. What problems might this cause? anaerobic metabolism to regenerate NAD+ lack of pyruvate for gluconeogenesis - hypoglycemia

  26. Fig. 4-23, p. 102

  27. Metabolic consequences • Acetaldehyde toxicity • Elevated NADH:NAD+ ratio • Metabolic competition • Induced metabolic tolerance • Elevates HDL in serum and lowers serum lipoproteins • Slowing development of smooth muscles in atherosclerosis

  28. Diseases of Carbohydrate Metabolism • Diabetes • Hypoglycemia

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