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Chapter 22b

Chapter 22b. Metabolism and Energy Balance. Homeostatic Control of Metabolism. Endocrine pancreas secretes hormones insulin and glucagon. These control blood sugar. Figure 22-8a. Homeostatic Control of Metabolism. Figure 22-8b. Homeostatic Control of Metabolism.

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Chapter 22b

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  1. Chapter 22b Metabolism and Energy Balance

  2. Homeostatic Control of Metabolism • Endocrine pancreas secretes hormones insulin and glucagon. These control blood sugar. Figure 22-8a

  3. Homeostatic Control of Metabolism Figure 22-8b

  4. Homeostatic Control of Metabolism • In the fed state, high levels of plasma glucose and amino acids result in the secretion of insulin. • Note effects of insulin √ Figure 22-9a

  5. Homeostatic Control of Metabolism • In the fasting state, low plasma glucose results in the secretion of glucagon • Note effects of glucagon √ Figure 22-9b

  6. Homeostatic Control of Metabolism • Levels of glucose, glucagon, and insulin vary over a typical 24-hour period Figure 22-10

  7. Factors That Control Insulin Secretion 1 - Increased plasma glucose 2 - Increased plasma amino acids 3 - Feedforward effects of GI hormones 4 - Parasympathetic activity 5 - Sympathetic activity

  8. Insulin Promotes Anabolism • Increases glucose transport into most, but not all, insulin-sensitive cells • Enhances cellular utilization and storage of glucose • Enhances utilization of amino acids • Promotes fat synthesis

  9. Glucose Uptake by Adipose Tissue and Resting Skeletal Muscle is Insulin-Sensitive • In the absence of insulin, glucose cannot enter cell Figure 22-12a

  10. Insulin Enables Glucose Uptake by Adipose Tissue and Resting Skeletal Muscle • Insulin signals the cell Figure 22-12b

  11. Insulin Indirectly Alters Glucose Transport in Hepatocytes • Hepatocyte in fed state Figure 22-13a

  12. Insulin Indirectly Alters Glucose Transport in Hepatocytes • Hepatocyte in fasted state Figure 22-13b

  13. Fed State: Insulin is an Anabolic Hormone KEY Plasmaglucose • Insulin promotes • Glucose uptake • Glucose metabolism • Energy storage as glycogen and fat Stimulus Integrating center Efferent path Effector  cellsof pancreas  cellsof pancreas Tissue response Systemic response Insulin Muscle, adipose,and other cells Liver Glucose transport Glycolysis Glycogenesis Lipogenesis Negativefeedback Plasmaglucose Figure 22-14

  14. Glucagon Is Dominant in the Fasted State • Glucagon is anatgonistic to most actions of insulin, resulting in a catabolic state in the body Figure 22-9b

  15. Endocrine Response to Hypoglycemia Figure 22-15

  16. Diabetes Mellitus is a Family of Diseases • Diabetes mellitus is a condition characterized by chronic elevated plasma glucose levels, or hyperglycemia • Diabetes is reaching epidemic proportions in the USA • Complications of diabetes affect many body systems • The two types of diabetes are • Type 1 - characterized by insulin deficiency • Type 2 - known as insulin-resistant diabetes (cells cannot respond to the insulin in the body)

  17. Acute Pathophysiology of Type 1 Diabetes Mellitus ACUTE PATHOPHYSIOLOGY OF TYPE 1 DIABETES MELLITUS FAT METABOLISM GLUCOSE METABOLISM PROTEIN METABOLISM Mealabsorbed • Overview • See pages 743 - 745 Plasmaamino acids Plasmafatty acids Plasmaglucose No insulin released Amino aciduptake bymost cells Protein breakdown,especially muscle Glucose uptake(muscle and adipose) Fatbreakdown Fatstorage Glucose utilization Liver Plasmaamino acids Plasmafatty acids Glycogenolysis Ketoneproduction Brain interpretsas starvation Gluconeogenesis Substratefor ATPproduction Substrate forATP production Hyperglycemia Polyphagia Tissueloss Tissueloss METABOLIC ACIDOSIS DEHYDRATION Exceeds renalthreshold for glucose Glucosuria Osmotic diuresisand polyuria Ventilation Metabolicacidosis Thirst Polydipsia Urineacidificationandhyperkalemia Dehydration ADH secretion Blood volume andBlood pressure Attempted compensationby cardiovascularcontrol center Lactic acidproduction Anaerobicmetabolism Circulatoryfailure compensationfails Coma ordeath Figure 22-16

  18. Acute Pathophysiology of Type 1 Diabetes Mellitus ACUTE PATHOPHYSIOLOGY OF TYPE 1 DIABETES MELLITUS FAT METABOLISM GLUCOSE METABOLISM PROTEIN METABOLISM Mealabsorbed 1 - Absorption of nutrients is normal Plasmaamino acids Plasmafatty acids Plasmaglucose Figure 22-16 (1 of 8)

  19. Acute Pathophysiology of Type 1 Diabetes Mellitus ACUTE PATHOPHYSIOLOGY OF TYPE 1 DIABETES MELLITUS FAT METABOLISM GLUCOSE METABOLISM PROTEIN METABOLISM Mealabsorbed 2a (protein) - Most cells unable to absorb nutrients shift to fasted state metabolism Plasmaamino acids Plasmafatty acids Plasmaglucose No insulin released Amino aciduptake bymost cells Protein breakdown,especially muscle Liver Plasmaamino acids Substratefor ATPproduction Tissueloss Figure 22-16 (2 of 8)

  20. Acute Pathophysiology of Type 1 Diabetes Mellitus ACUTE PATHOPHYSIOLOGY OF TYPE 1 DIABETES MELLITUS FAT METABOLISM GLUCOSE METABOLISM PROTEIN METABOLISM Mealabsorbed 2b (fat) - Most cells unable to absorb nutrients shift to fasted state metabolism Plasmaamino acids Plasmafatty acids Plasmaglucose No insulin released Amino aciduptake bymost cells Protein breakdown,especially muscle Fatbreakdown Fatstorage Liver Plasmaamino acids Plasmafatty acids Ketoneproduction Substratefor ATPproduction Substrate forATP production Tissueloss Tissueloss Figure 22-16 (3 of 8)

  21. Acute Pathophysiology of Type 1 Diabetes Mellitus ACUTE PATHOPHYSIOLOGY OF TYPE 1 DIABETES MELLITUS FAT METABOLISM GLUCOSE METABOLISM PROTEIN METABOLISM Mealabsorbed 3 - Hyperglycemia results when liver cells also shift to the fasted state, and produce more glucose! Plasmaamino acids Plasmafatty acids Plasmaglucose No insulin released Amino aciduptake bymost cells Protein breakdown,especially muscle Glucose uptake(muscle and adipose) Fatbreakdown Fatstorage Glucose utilization Liver Plasmaamino acids Plasmafatty acids Glycogenolysis Ketoneproduction Gluconeogenesis Substratefor ATPproduction Substrate forATP production Hyperglycemia Tissueloss Tissueloss Figure 22-16 (4 of 8)

  22. Acute Pathophysiology of Type 1 Diabetes Mellitus ACUTE PATHOPHYSIOLOGY OF TYPE 1 DIABETES MELLITUS FAT METABOLISM GLUCOSE METABOLISM PROTEIN METABOLISM Mealabsorbed 3b – More glucose results in polyphagia Plasmaamino acids Plasmafatty acids Plasmaglucose No insulin released Amino aciduptake bymost cells Protein breakdown,especially muscle Glucose uptake(muscle and adipose) Fatbreakdown Fatstorage Glucose utilization Liver Plasmaamino acids Plasmafatty acids Glycogenolysis Ketoneproduction Brain interpretsas starvation Gluconeogenesis Substratefor ATPproduction Substrate forATP production Hyperglycemia Polyphagia Tissueloss Tissueloss Figure 22-16 (5 of 8)

  23. Acute Pathophysiology of Type 1 Diabetes Mellitus ACUTE PATHOPHYSIOLOGY OF TYPE 1 DIABETES MELLITUS FAT METABOLISM GLUCOSE METABOLISM PROTEIN METABOLISM Mealabsorbed 4a - Hyperglycemia results in glucose in the urine and increased urine production Plasmaamino acids Plasmafatty acids Plasmaglucose No insulin released Amino aciduptake bymost cells Protein breakdown,especially muscle Glucose uptake(muscle and adipose) Fatbreakdown Fatstorage Glucose utilization Liver Plasmaamino acids Plasmafatty acids Glycogenolysis Ketoneproduction Brain interpretsas starvation Gluconeogenesis Substratefor ATPproduction Substrate forATP production Hyperglycemia Polyphagia Tissueloss Tissueloss Exceeds renalthreshold for glucose Glucosuria Osmotic diuresisand polyuria Figure 22-16 (6 of 8)

  24. Acute Pathophysiology of Type 1 Diabetes Mellitus ACUTE PATHOPHYSIOLOGY OF TYPE 1 DIABETES MELLITUS FAT METABOLISM GLUCOSE METABOLISM PROTEIN METABOLISM Mealabsorbed 4b – And then low blood pressure as a result of dehydration Plasmaamino acids Plasmafatty acids Plasmaglucose No insulin released Amino aciduptake bymost cells Protein breakdown,especially muscle Glucose uptake(muscle and adipose) Fatbreakdown Fatstorage Glucose utilization Liver Plasmaamino acids Plasmafatty acids Glycogenolysis Ketoneproduction Brain interpretsas starvation Gluconeogenesis Substratefor ATPproduction Substrate forATP production Hyperglycemia Polyphagia Tissueloss Tissueloss DEHYDRATION Exceeds renalthreshold for glucose Glucosuria Osmotic diuresisand polyuria Thirst Polydipsia Dehydration ADH secretion Blood volume andBlood pressure Attempted compensationby cardiovascularcontrol center Figure 22-16 (7 of 8)

  25. Acute Pathophysiology of Type 1 Diabetes Mellitus ACUTE PATHOPHYSIOLOGY OF TYPE 1 DIABETES MELLITUS FAT METABOLISM GLUCOSE METABOLISM PROTEIN METABOLISM Mealabsorbed 5 - Metabolic acidosis results, which if untreated can lead to coma and/or death Plasmaamino acids Plasmafatty acids Plasmaglucose No insulin released Amino aciduptake bymost cells Protein breakdown,especially muscle Glucose uptake(muscle and adipose) Fatbreakdown Fatstorage Glucose utilization Liver Plasmaamino acids Plasmafatty acids Glycogenolysis Ketoneproduction Brain interpretsas starvation Gluconeogenesis Substratefor ATPproduction Substrate forATP production Hyperglycemia Polyphagia Tissueloss Tissueloss METABOLIC ACIDOSIS DEHYDRATION Exceeds renalthreshold for glucose Glucosuria Osmotic diuresisand polyuria Ventilation Metabolicacidosis Thirst Polydipsia Urineacidificationandhyperkalemia Dehydration ADH secretion Blood volume andBlood pressure Attempted compensationby cardiovascularcontrol center Lactic acidproduction Anaerobicmetabolism Circulatoryfailure compensationfails Coma ordeath Figure 22-16 (8 of 8)

  26. Type 2 Diabetes • Accounts for 90% of all diabetics • Insulin resistance (target cells do not respond normally) • Early symptoms are mild, but later complications include atherosclerosis, neurological changes, renal failure, and blindness • Therapy • Diet and physical exercise • Drugs

  27. Glucose Tolerance Test Figure 22-17

  28. Drugs Attempt to Treat Diabetes by Varying Mechanisms Table 22-6

  29. Metabolic Syndrome - Insulin resistance syndrome • Patients have combined symptoms of type 2 diabetes, atherosclerosis, and high blood pressure • Diagnostic criteria - three or more of • Central (visceral) obesity • Blood pressure ≥ 130/85 mm Hg • Fasting blood glucose ≥ 110 mg/dL • Elevated fasting plasma triglyceride levels • Low plasma HDL-C levels

  30. Fats • Assembled into chylomicrons in SI lining • Into lymphatics to blood to liver • Liver processes into lipoproteins LDL’s • LDL’s to cells for use in synthesis of cholesterol • Likely leads to atherosclerosis • HDL’s depleted of cholesterol tend to return to liver for processing into bile for excretion – lowers cholesterol • HMG coAreductase inhibitors – Big $$ • statins – lipitorlovastatin also other cholesterol treatments: fibrates and niacin

  31. Fat catabolism • Ketosis • Excessive leads to metabolic acidosis • FA catabolized into ketone bodies two carbons at a time – ß - oxidation

  32. Body Temperature: Energy Balance in the Body ENERGY INPUT ENERGY OUTPUT DIET• Hunger/appetite• Satiety• Social and psychological factors HEAT (~50%) • Unregulated • Thermoregulation WORK (~50%)• Transport across membranes • Mechanical work Movement• Chemical work • Synthesis for growth and maintenance • Energy storage• High-energy phosphate bonds (ATP, phosphocreatine)• Chemical bonds (glycogen, fat) Figure 22-18

  33. Body Temperature: Heat Balance in the Body EXTERNAL HEAT INPUT + INTERNAL HEAT PRODUCTION = HEAT LOSS Evaporation Radiation Radiation heat loss heat input Conduction Body heat Conduction Convection Internalheatproduction heat production Frommetabolism From musclecontraction “Wasteheat” ? Nonshiveringthermogenesis Shiveringthermogenesis “Wasteheat” Regulated processesfor temperature homeostasis Figure 22-19

  34. Body Temperature: Thermoregulatory Reflexes Figure 22-20 (1 of 2)

  35. Body Temperature: Thermoregulatory Reflexes Figure 22-20 (2 of 2)

  36. Mechanisms of Body Temperature Regulation • Neural control of cutaneous blood flow alters heat loss through the skin • Sweat contributes to heat loss • Heat production • Voluntary muscle contraction and normal metabolism • Regulated heat production • Shivering versus nonshivering thermogenesis

  37. Homeostatic Responses to High Temperature Figure 22-21 (1 of 2)

  38. Homeostatic Responses to Low Temperature Figure 22-21 (2 of 2)

  39. Regulation of Body Temperature • Our hypothalamic thermostat can be reset • Typical physiological variations • Fever occurs when pyrogensreset the thermostat • Pathological cases of altered body temperature • Hyperthermia - compare • Heat exhaustion • Heat stroke • Heat exhaustion is characterized by significant sweating, loss of color, cramps, fatigue, fainting and dizziness. • Heat stroke symptoms include a body temperature over 103, dry skin, high heart rate, confusion and even unconsciousness • Malignant hyperthermia • Hypothermia • Diving reflex √

  40. Summary • Appetite and Satiety • Feeding and satiety centers, glucostatic versus lipostatic theories, regulation of food intake by numerous regulatory peptides • Energy Balance • Definition of energy balance, bodily uses for energy, direct calorimetry, oxygen consumption, RQ, RER, BMR, diet-induced thermogenesis, glycogen and fat as two major forms of stored energy

  41. Summary • Metabolism • Anabolic pathways versus catabolic pathways, fed state versus fasted state, glycogenesis, glycogenolysis, and gluconeogenesis • Chylomicrons, lipoprotein lipase, apoproteins A and B, LDL-C, risks factors for heart disease, beta oxidation and ketone bodies

  42. Summary • Homeostatic Control of Metabolism • Ratio of insulin to glucagon, Islets of Langerhans, insulin-receptor substrates, major targets and effects of insulin, glucagon and the fasted state, diabetes mellitus, and metabolic syndrome • Regulation of body temperature • Hypothalamic thermostat, routes and mechanisms of heat loss, shivering thermogenesis and nonshivering thermogenesis

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