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Chapter 19

Chapter 19. Regulation of Metabolism. 19-1. Chapter 19 Outline Nutrition & Metabolism Regulation of Metabolism & Hunger Energy Regulation by Islets of Langerhans Diabetes Mellitus & Hypoglycemia Metabolic Regulation by Adrenal Hormones, Thyroxine, & GH

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Chapter 19

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  1. Chapter 19 Regulation of Metabolism 19-1

  2. Chapter 19 Outline • Nutrition & Metabolism • Regulation of Metabolism & Hunger • Energy Regulation by Islets of Langerhans • Diabetes Mellitus & Hypoglycemia • Metabolic Regulation by Adrenal Hormones, Thyroxine, & GH • Regulation of Calcium & Phosphate Balance 19-2

  3. Nutrition & Metabolism 19-3

  4. Nutritional Requirements • Living tissue is maintained by constant expenditure of energy (ATP) • ATP derived from glucose, fatty acids, ketones, amino acids, & others • Energy of food is commonly measured in kilocalories (1 kcal = 1000 calories) • Carbohydrates & proteins yield 4kcal/gm; fats-9kcal/gm 19-4

  5. Metabolic Rate & Caloric Requirements • Metabolic rate (MR) is total rate of body metabolism • = amount of O2 consumed by body/min • Basal metabolic rate (BMR) is MR of awake relaxed person 12–14 hrs after eating & at a comfortable temperature • BMR depends on age, sex, body surface area, activity level, & thyroid hormone levels • Hyperthyroids have high BMR; hypothyroids have low BMR 19-5

  6. Metabolism • Is all chemical reactions in body • Includes synthesis & energy storage reactions (anabolism); & energy liberating reactions (catabolism) 19-6

  7. Anabolic Requirements • Anabolic reactions synthesize DNA & RNA, proteins, fats, & carbohydrates • Must occur constantly to replace molecules that are hydrolyzed in catabolic reactions 19-7

  8. Turnover Rate • Is rate at which a molecule is broken down & resynthesized • Average turnover for Carbs is 250 g/day • Some glucose is reused so net need ≈150 g/day • Average turnover for protein is 150 g/day • Some is reused for protein synthesis so net need ≈35 g/day • 9 essential amino acids must be supplied in diet because can't be synthesized 19-8

  9. Turnover Rate continued • Average turnover for fats is 100 g/day • Little is required in diet because can be synthesized from Carbs • 2 essential fatty acids must be supplied in diet 19-9

  10. Vitamins • Are small organic molecules that serve as coenzymes in metabolism or have highly specific functions • Must be obtained in diet because body does not produce them, or does so in insufficient amounts • Can be placed in 2 classes • Fat-solubles include A, D, E, & K • Water-solubles include B1, B2, B3, B6, B12, pantothenic acid, biotin, folic acid, & vitamin C • Serve as coenzymes in metabolism 19-10

  11. 19-11

  12. Minerals (Elements) • Are needed as cofactors for specific enzymes & other critical functions • Sodium, potassium, magnesium, calcium, phosphate, & chloride are needed daily in large amounts • Iron, zinc, manganese, fluorine, copper, molybdenum, chromium, & selenium are trace elements required in small amounts/day 19-12

  13. Free Radicals • Are highly reactive & oxidize or reduce other atoms • Because have an unpaired electron in their outer orbital • The major free radicals are reactive oxygen or reactive nitrogen species • Because contain oxygen or nitrogen with unpaired electron • Include NO radical, superoxide radical, & hydroxyl radical 19-13

  14. Free Radicals continued • Serve important physiological functions • Help to destroy bacteria • Can produce vasodilation • Can stimulate cell proliferation 19-14

  15. Free Radicals continued • In excess can exert oxidative stress contributing to disease states • Can damage lipids, proteins, & DNA • Promotes apoptosis, aging, inflammatory disease, degenerative, & other diseases & malignant growth • Underlying cause is widespread production of superoxide radicals by mitochondria 19-15

  16. Free Radicals continued • Body uses enzymatic & nonezymatic means to protect itself against oxidative stress • Enzymes that neutralize free radicals include superoxide dismutase (SOD), catalase, & glutathione peroxidase • Nonenzymes that react with free radicals by picking up unpaired electrons include glutathione, vitamin C, & vitamin E 19-16

  17. Fig 19.1: Reactive Oxygen Species Balance 19-17

  18. Regulation of Metabolism & Hunger 19-18

  19. Regulation of Energy Metabolism • Blood contains glucose, fatty acids, amino acids, & others that can be used for energy • These can be circulating energy substrates from digestion or energy reserves (glycogen, protein, or fat) Fig 19.2 19-19

  20. Control of Adipose Tissue Levels • Body appears to have negative feedback loops (an adipostat) to defend maintenance of a certain amount of adipose tissue • Adipose cells (adipocytes) store & release fat under hormonal control • And may release their own hormone(s) to influence metabolism 19-20

  21. Development of Adipose Tissue • Number of adipocytes increases greatly after birth • Due to mitosis & differentiation of preadipocytes into adipocytes • Differentiation promoted by high levels of fatty acids • Requires nuclear receptor protein (PPARg) that is activated when bound to a prostaglandin or drugs 19-21

  22. Endocrine Functions of Adipocytes • Adipocytes secrete regulatory factors when their PPARg receptors are activated • Which cause muscle to become more responsive to insulin • PPARg-activating drugs are used to treat Type II diabetes 19-22

  23. Endocrine Functions of Adipocytes cont. • The adipocyte hormones TNFa, resistin, & leptin are increased in obesity & Type II diabetes • All appear to reduce sensitivity of muscle to insulin (insulin resistance) • Leptin signals hypothalamus how much fat is stored, regulating hunger & food intake 19-23

  24. Low Adiposity: Starvation • Starvation & malnutrition diminish immune function • Low adipose levels cause low leptin levels • Helper T cells have leptin receptors • Thus low leptin can lead to diminished immune function • Leptin may play role in timing of puberty & in amenorrhea of underweight women 19-24

  25. Obesity • Childhood obesity involves increases in both size & number of adipocytes • Weight gain in adulthood is due mainly to increase in adipocyte size 19-25

  26. Obesity continued • Obesity is often diagnosed by using using a body mass index (BMI) • BMI = w h2 • w = weight in kilograms • h = height in meters • Healthy weight is BMI between 19 – 25 • Obesity defined as BMI > 30 19-26

  27. Regulation of Hunger • Is at least partially controlled by hypothalamus • Lesions in ventromedial area produce hyperphagia & obesity in animals • Lesions in lateral area produce hypophagia • Involves a number of NTs: endorphins (promote overeating), Norepi (promotes overeating), serotonin (suppresses overeating) • Very successful diet pills Redux & fen-phen worked by elevating brain serotonin • (Now banned because of heart valve side effects) 19-27

  28. Regulation of Hunger continued • Involves arcuate nucleus of hypothalamus • Its neurons send axons to paraventricular nucleus & lateral hypothalamus • 1 type of neurons produce MSH which suppresses hunger • Another produces neuropeptide Y & agouti-related peptidewhich increase hunger 19-28

  29. Regulation of Hunger continued • Involves signals from stomach & SI • Ghrelin stimulates hunger via effect in arcuate • Secreted by stomach at high levels when stomach is empty & low levels when full • CCK from SI promotes satiety • Levels rise during & immediately after a meal • Ghrelin & CCK regulate hunger on short-term, meal-to-meal basis 19-29

  30. Regulation of Hunger continued • PYY is secreted by SI in proportion to caloric content of food • Decreases hunger by acting in arcuate to decrease neuropeptide Y & stimulate MSH • Seems to serve intermediate level of control because injections reduce appetite for 12 hrs 19-30

  31. Regulation of Hunger continued • Is influenced by leptin--a satiety factor secreted by adipocytes & involved in long-term regulation • Secretion increases as stored fat increases • Signals body's level of adiposity • Acts in arcuate to suppress Neuropep Y & agouti-related peptide; & stimulate MSH • Insulin may play role in satiety • Suppresses Neuropep Y 19-31

  32. Fig 19.3 19-32

  33. Calorie Expenditure of Body • Has 3 components: • Number of calories used at BMR make up 60% of total • Number used in response to temperature changes & during digestion/absorption (adaptive thermogenesis) make-up 10% of total • Starvation can lower MR 40%; eating raises MR 25-40% (thermic effect of food) • Number used during physical activity depends on type & intensity 19-33

  34. Absorptive & Postabsorptive States • Absorptive state is 4 hr period after eating • Energy substrates from digestion are used & deposited in storage forms (anabolism) • Postabsorptive or fasting state follows absorptive state • Energy is withdrawn from storage (catabolism) 19-34

  35. Hormonal Regulation of Metabolism • Balance between anabolism & catabolism depends on levels of insulin, glucagon, GH, thyroxine, & others Fig19.5 19-35

  36. 19-36

  37. Fig 19.6 19-37

  38. Energy Regulation by Islets of Langerhans 19-38

  39. Pancreatic Islets of Langerhans • Contain 2 cell types involved in energy homeostasis: • a cells secreteglucagon when glucose levels are low • Which causes increased glucose by stimulating glycogenolysis in liver • b cells secreteinsulin when glucose levels are high • Which reduces blood glucose by promoting its uptake by tissues 19-39

  40. Insulin & Glucagon Secretion • Normal fasting glucose level is 65–105 mg/dl • Insulin & glucagon normally prevent levels from rising above 170mg/dl after meals or falling below 50mg/dl between meals Fig 19.7 19-40

  41. Insulin • Overall effect is to promote anabolism • Promotes storage of digestion products • Inhibits breakdown of fat & protein • Inhibits secretion of glucagon • Stimulates insertion of GLUT4 transporters in cell membrane of skeletal muscle, liver, & fat • Transports by facilitated diffusion 19-41

  42. Oral Glucose Tolerance Test • Measures response to drinking a glucose solution • Assesses ability of b cells to secrete insulin & insulin's ability to lower blood glucose • In non-diabetics, glucose levels return to normal within 2 hrs Insert fig. 19.8 Fig 19.9 19-42

  43. Glucagon • Maintains blood glucose concentration above 50mg/dl • Stimulates glycogenolysis in liver • Stimulates gluconeogenesis, lipolysis, & ketogenesis • Skeletal muscle, heart, liver, & kidneys use fatty acids for energy 19-43

  44. Fig 19.10 19-44

  45. Effects of ANS on Insulin & Glucagon • ANS innervates islets • Activation of Parasymp NS stimulates insulin secretion • Activation of Symp NS stimulates glucagon & inhibits insulin • This can cause "stress hyperglycemia" 19-45

  46. Effects of Intestinal Hormones • Insulin levels increase more after glucose ingestion than after intravenous glucose infusion • Due to hormones secreted by intestine during meals "in anticipation" of glucose rise • GIP, GLP-1, & CCK all stimulate insulin secretion 19-46

  47. Effect of Feeding & Fasting on Metabolism Fig 19.11 19-47

  48. Diabetes Mellitus & Hypoglycemia 19-48

  49. Diabetes Mellitus • Characterized by chronic high blood glucose levels (hyperglycemia) • Type I (insulin dependent or IDDM) is due to insufficient insulin secretion • Type II (insulin independentor NIDDM) is due to lack of effect of insulin 19-49

  50. 19-50

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