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XIV. PANCREATIC HORMONES

XIV. PANCREATIC HORMONES. Diabetes mellitus - 16 million in U.S., half unaware, 650,000 new diagnoses/year Occurs most often in adults But is most prevalent chronic disorder in teenagers — 127,000. 1. Insulin - secreted by ß-cells 2. Glucagon - secreted by  -cells

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XIV. PANCREATIC HORMONES

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  1. XIV. PANCREATIC HORMONES Diabetes mellitus - 16 million in U.S., half unaware, 650,000 new diagnoses/year Occurs most often in adults But is most prevalent chronic disorder in teenagers — 127,000 1. Insulin - secreted by ß-cells2. Glucagon - secreted by -cells 3. Both hormones regulate blood glucose levels A. Hormones

  2. XIV. PANCREATIC HORMONES A. Regulation of release 1. Gastrointestinal nutrients and hormones — glucose, amino acids, fatty acids, ketone bodies and gastrointestinal hormones stimulate secretion. 2. Autonomic mechanisms --Norepinephrine and epinephrine inhibit secretionSelective ß-receptor stimulation stimulates releaseCholinergic stimulation (e.g., vagus) stimulates release 3. Hormonesa) glucagonb) somatostatin 4. Glucose — increase in blood glucose increases release decrease in blood glucose decreases release

  3. Glucose ATP Glucose Metabolism Insulin XIV. PANCREATIC HORMONES B. Mechanism of release Leads to depolarization Decreases potassium conductance Glucose transporter Closes Potassium channel Calcium channels R Ca+ Insulin granules

  4. Glucagon Glucose Glycogen synthetase Glycogen Gluco-1- phosphatase Energy utilization Gluconeogenesis Free Fatty Acids Lipase Ketone Bodies Protein Urea excretion Liver Lipid Amino Acids XIV. PANCREATIC HORMONES C. Role in metabolic processes 1. Review R

  5. Glucose Glycogen synthetase Glycogen Gluco-1- phosphatase Energy utilization Gluconeogenesis Ketone Bodies Lipase Free Fatty Acids Protein Urea excretion Liver Lipid Amino Acids XIV. PANCREATIC HORMONES C. Role in metabolic processes 2. Insulin effects Increases Decreases Insulin R

  6. Lipase Free Fatty Acids XIV. PANCREATIC HORMONES C. Role in metabolic processes 3. Insulin deficiency Hyperglycemia Increases Decreases Glycogen synthetase Insulin R Glycogen (Ketonemia and Acidosis) Gluco-1- phosphatase Energy utilization Gluconeogenesis Ketone Bodies Urea excretion (Azoturia) Protein Liver Lipid Amino Acids Hyperlipemia

  7. XIV. PANCREATIC HORMONES D. Types of diabetes mellitus 1. Insulin-dependent diabetes mellitus (IDDM, Type I)a) Characteristics: Severe form Usually in juveniles Occasionally in adults Insulin virtually absent Plasma glucagon elevated b) Etiology Pancreatic B cell unresponsive to insulin stimuli Damaged pancreatic B cells Autoimmune response Environmental insult Genetic defect

  8. XIV. PANCREATIC HORMONES D. Types of diabetes mellitus • 2. Non-insulin-dependent diabetes mellitus (NIDDM, Type II) • a) Characteristics: • Milder than IDDM • Usually adults, occasionally juveniles • Heterogenous group • b) Etiology • Subnormal levels of insulin • Tissue insensitivity to insulin • Pancreatic B cell unresponsive to insulin • Hyperglycemia impairs B cell response

  9. XIV. PANCREATIC HORMONES E. Replacement therapy in IDDM 1. Preparations of insulin are divided into three catagories according to promptness, duration and intensity of action.2. Fast-acting — zinc insulin 3. Intermediate acting — Isophane insulin suspension is a modified protamine zinc insulin suspension4. Long-acting -- Hagedorn insulin-zinc-protamine complex 5. Humalog Mix 25 (Canada) 6. Velosulin BR 5. New modes of treatment - infusion pumps and inhalers

  10. XIV. PANCREATIC HORMONES F. Insulin side effects 1. Hypoglycemia — insulin requirement reduced, failure to eat, unaccustomed exercise, or insulin overdose can all cause hypoglycemia a) A rapid fall in blood glucose b) A slow fall in blood glucose Treatment of hypoglycemia is to administer fruit juice or glucose; if not available, then glucagon2. Other adverse reactions — mostly allergic reactions, but usually subside after chronic administration

  11. XIV. PANCREATIC HORMONES G. Treatment of NIDDM 1. Diet 2. Insulin -- most patients treated with insulin and diet3. Oral hypoglycemic agents: Used when diet control insufficient Used with insulin to lower dosage of insulin. Not when insulin requirements exceed 200 units/day.

  12. G. Treatment of NIDDM XIV. PANCREATIC HORMONES 3. Oral hypoglycemic agents (cont.) a) Sulfonylureas (first generation) 1) Agents - acetohexamide (Dymelor), chlorpropamide (Diabinese), tolazamide (Tolinase), tolbutamide (Orinase) 2) Mechanism of action -- stimulate ß-cells to secrete insulin 3) Adverse effects -- associated with cardiovascular disease, hypoglycemia Effectiveness questioned b) Sulfonylureas (second generation) a) Agents - glyburide (Diabeta, Micronase) and glipizide (Glucotrol) and Glimepride (1996) b) Mechanism of action: Stimulate insulin release from ß cells (K channel blockers) Release glucogon and somatostatin Inhibit hepatic gluconeogenesis Enhance insulin receptor sensitivity c) Adverse effects - less than with first generation

  13. XIV. PANCREATIC HORMONES G. Treatment of NIDDM c) Biguanides Phenformin introduced in 1957 Metformin (Glucophage) available in 1994 Mechanism of action -- increases the utilization of glucose by decreasing cellular respiration decreases glucose levels by inhibiting gluconeogenesis inhibits intestinal absorption of glucose Adverse effects -- phenformin produced fatal lactic acidosis, metformin much less so Contraindications — hepatic disease or past history of lactic acidosis

  14. XIV. PANCREATIC HORMONES G. Treatment of NIDDM d) Thiazolidinediones (antihyperglycemic) Troglitazone (Rezulin) - marketed in 1997 Ciglitazone, Pioglitazone (Actos) - FDA approval pending, Rosiglitazone (Avandia) Action - reduce plasma glucose, insulin and lipid levels in insulin-rresistant animal models Mechanism of action - increases synthesis of insulin transporters Toxicity - troglitazone implicated in acute liver failure, FDA recommends other in this class carry warning label rosiglitazone elevates LDL rosiglitazone may be fetotoxic

  15. XIV. PANCREATIC HORMONES G. Treatment of NIDDM e) Alpha-glucosidase inhibitors Acarbose (Precose) Mechanism of action - reduces intestinal absorption of starch dextrin, and disaccharides — postprandial reduction in plasma glucose Side effects - malabsorption, flatulence and abdominal bloating

  16. XIV. PANCREATIC HORMONES H. Glucagon 1. Physiological actions a) Insulin and glucagon are mutual antagonists Glucagon mobilizes fuel -- increases [glucose] plasma Increased glucose leads to increase in insulin and decrease in glucagon b) Following a meal, decreased glucagon secretion. c) Starvation (decrease in blood glucose) causes increase in glucagon secretion2. Regulation of secretion -- glucose is primary stimulus. Increased plasma glucose decreases glucagon secretion and vice versa3. Therapeutic use -- used to treat insulin-induced hypoglycemia

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