L24 NPB 101 - Lecture 24 •  SmartSite: – ...

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Unformatted text preview: Lecture 24 •  SmartSite: –  Lecture 24 Notes •  Review •  Endocrinology –  Pancreas (Con<nued) –  Calcium Metabolism •  Announcements: –  None •  Reading (Recommended): –  Relevant por<ons Chapter 19 1 REV: •  Adrenal –  Cor<cal Hormones •  Cor<sol – Major metabolic and stress hormone •  Aldosterone – Regula<on of K+ and Na+ concentra<ons •  DHEA  ­ Only adrenal sex hormone of any biological importance •  Catecholamines – Modified SNS & epinephrine release –  Medullary Hormones •  Stress Response (GAS) •  Endocrine control of Fuel Metabolism •  Pancreas –  Nonspecific generalized response preparing for “fight or flight” –  Involves mul<ple hormone systems: cor<sol, SNS/Epinephrine, ADH, Aldosterone, Glucagon & Insulin –  Degrada<on, synthesis, and transforma<on of proteins, carbohydrates, and fats –  Endocrine & Exocrine Gland 2 Pancrea<c Pep<de Hormones •  Endocrine cells of the Pancreas – Islets of Langerhans –  β (beta) cells –  α (alpha) cells –  D (delta) cells •  Insulin synthesis & secre<on •  Glucagon synthesis & secre<on •  Somatosta<n synthesis & secre<on •  modulates insulin/glucagon secre<on •  Least common islet cells •  Secrete pancrea<c polypep<de –  PP cells •  Insulin and glucagon Fig. 19 ­15, pg. 715 –  Most important in regula<ng fuel metabolism 3 Pancrea<c Hormones •  Insulin –  Anabolic hormone –  Promotes cellular uptake of glucose, faby acids, and amino acids and enhances their conversion into glycogen, triglycerides, and proteins, respec<vely •  Lowers blood concentra<on of these small organic molecules –  Secre<on is increased during absorp<ve state •  Primary s<mulus for secre<on is increase in blood glucose concentra<on 4 Glucose S<mula<on of Insulin Secre<on Fig. 19 ­17, pg. 718 5 Factors controling insulin secre<on * * Glucose ­dependent insulinotropic pep<de (GIP) Fig. 19 ­18, pg. 719 6 Diabetes Mellitus •  Most common of all endocrine disorders –  2005 Es<mated 20.8 million people—7% of the US popula<on •  Prominent feature is elevated blood glucose levels –  Urine acquires sweetness from excess blood glucose that spills into urine –  Type I diabetes •  Two major types •  Characterized by lack of insulin secre<on •  Characterized by normal or even increased insulin secre<on but reduced sensi<vity of insulin’s target cells 7 –  Type II diabetes Comparison of Type I and Type II Diabetes Must be careful not to drive glucose levels too low Table, pg. 721 8 Acute Effects of Diabetes Mellitus Fig. 19 ­19, pg. 722 9 Pancrea<c Hormones •  Glucagon –  Mobilizes energy ­rich molecules from storage sites during postabsorp<ve state –  Secreted in response to a decrease in blood glucose on pancrea<c α cells –  Generally opposes ac<ons of insulin –  No known clinical abnormali<es caused by glucagon deficiency or excess •  Excess of glucose can aggravate hyperglycemia of diabetes mellitus 10 Summary of Hormonal Control of Fuel Metabolism Table 19 ­6, pg. 726 11 Calcium Metabolism 12 Endocrine Control of Calcium Metabolism •  Plasma Ca2+ must be closely regulated to prevent changes in neuromuscular excitability –  Also plays vital role in a number of essen<al ac<vi<es •  •  •  •  Excita<on ­contrac<on coupling in cardiac and smooth muscle S<mulus ­secre<on coupling Maintenance of <ght junc<ons between cells Cloong of blood –  Hypercalcemia •  Reduces excitability –  Hypocalcemia •  Brings about overexcitability of nerves and muscles •  Severe overexcitability can cause fatal spas<c contrac<ons of respiratory muscles 13 Func<ons of the Skeleton Table 19 ­7, pg. 728 14 Endocrine Control of Calcium Metabolism •  Three hormones regulate plasma concentra<on of Ca2+ (and PO43 ­) –  Parathyroid hormone (PTH) –  Calcitonin –  Vitamin D 15 Endocrine Control of Calcium Metabolism •  Parathyroid hormone (PTH) –  Secreted by parathyroid glands –  Primary regulator of Ca2+ •  Raises free plasma Ca2+ levels by its effects on bone kidneys, and intes<nes –  Essen<al for life •  Prevents fatal consequences of hypocalcemia –  Facilitates ac<va<on of Vitamin D 16 Endocrine Control of Calcium Metabolism •  Calcitonin –  Hormone produced by C cells of thyroid gland –  Nega<ve ­feedback fashion •  Secreted in response to increase in plasma Ca2+ concentra<on –  Acts to lower plasma Ca2+ levels by inhibi<ng ac<vity of bone osteoclasts –  Unimportant except during hypercalcemia 17 Nega<ve ­feedback Loops Controlling PTH and Calcitonin Secre<on Fig. 19 ­25, pg. 734 18 Endocrine Control of Calcium Metabolism •  Vitamin D –  S<mulates Ca2+ and PO43 ­ absorp<on from intes<ne –  Can be synthesized from cholesterol deriva<ve when exposed to sunlight •  Oqen inadequate source –  Amount supplemented by dietary intake –  Must be ac<vated first by liver and then by kidneys before it can exert its effect on intes<nes 19 Ac<va<on of vitamin D Fig. 19 ­26, pg. 735 20 Calcium Disorders •  PTH hypersecre<on (hyperparathyroidism) –  Characterized by hypercalcemia and hypophosphatemia •  PTH hyposecre<on (hypoparathyroidism) –  Characterized by hypocalcemia and hyperphosphatemia •  Vitamin D deficiency –  Children – rickets –  Adults – osteomalacia 21 ...
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This note was uploaded on 11/07/2010 for the course NPB NPB 101 taught by Professor Weidner/wingfield during the Spring '08 term at UC Davis.

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