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PowerPoint ® Lecture Slides prepared by Janice Meeking, Mount Royal College C H A P T E R Copyright © 2010 Pearson Education, Inc. 24 Nutrition, Metabolism, and Body Temperature Regulation: Part B
Copyright © 2010 Pearson Education, Inc. Protein Metabolism When dietary protein is in excess, amino acids are Oxidized for energy Converted into fat for storage
Copyright © 2010 Pearson Education, Inc. Oxidation of Amino Acids First deaminated; then converted into Pyruvic acid A keto acid intermediate of the Krebs cycle Events include transamination, oxidative deamination, and keto acid modification
Copyright © 2010 Pearson Education, Inc. Figure Krebs cycle Oxidative deamination Transamination Amino acid + Keto acid ( -keto- glutaric acid) Keto acid + Amino acid (glutamic acid) Keto acid modification Modified keto acid Enter Krebs cycle in body cells Liver Kidney Blood During transamination an amine group is switched from an amino acid to a keto acid. During keto acid modification the keto acids formed during transamination are altered so they can easily enter the Krebs cycle pathways. NH 3 (ammonia) Urea In oxidative deamination, the amine group of glutamic acid is removed as ammonia and combined with CO 2 to form urea. CO Excreted in urine
Copyright © 2010 Pearson Education, Inc. Protein Synthesis Is hormonally controlled Requires a complete set of amino acids Essential amino acids must be provided in the diet
Copyright © 2010 Pearson Education, Inc. Catabolic-Anabolic Steady State A dynamic state in which Organic molecules (except DNA) are continuously broken down and rebuilt Organs have different fuel preferences
Copyright © 2010 Pearson Education, Inc. Nutrient Pools Three interconvertible pools Amino acids Carbohydrates Fats
Copyright © 2010 Pearson Education, Inc. Amino Acid Pool Body’s total supply of free amino acids Source for Resynthesizing body proteins Forming amino acid derivatives Gluconeogenesis
Copyright © 2010 Pearson Education, Inc. Figure Pool of carbohydrates and fats (carbohydrates fats) Dietary proteins and amino acids Food intake Some lost via cell sloughing, hair loss Excreted in urine Some lost via surface secretion, cell sloughing Excreted via lungs Dietary carbohydrates and lipids Urea Components of structural and functional proteins Nitrogen-containing derivatives (e.g., hormones, neurotransmitters) Structural components of cells (membranes, etc.) Specialized derivatives (e.g., steroids, acetylcholine); bile salts Catabolized for energy Storage forms Pool of free amino acids NH 3 CO 2
Copyright © 2010 Pearson Education, Inc. Carbohydrate and Fat Pools Easily interconverted through key intermediates Differ from the amino acid pool in that: Fats and carbohydrates are oxidized directly to produce energy Excess carbohydrate and fat can be stored
Copyright © 2010 Pearson Education, Inc. Figure Proteins CarbohydratesFats Excreted in urine Glycogen Glucose Glucose-6-phosphate Glyceraldehyde phosphate Pyruvic acid Acetyl CoA Amino acids Keto acids Triglycerides (neutral fats) Lactic acid Ketone bodies Glycerol and fatty acids NH 3 Krebs cycle Urea
Copyright © 2010 Pearson Education, Inc. Absorptive and Postabsorptive States Absorptive (fed) state During and shortly after eating Absorption of nutrients is occurring Postabsorptive (fasting) state When the GI tract is empty Energy sources are supplied by breakdown of reserves
Copyright © 2010 Pearson Education, Inc. Absorptive State Anabolism exceeds catabolism Carbohydrates Glucose is the major energy fuel Glucose is converted to glycogen or fat
Copyright © 2010 Pearson Education, Inc. Absorptive State Fats Lipoprotein lipase hydrolyzes lipids of chylomicrons in muscle and fat tissues Most glycerol and fatty acids are converted to triglycerides for storage Triglycerides are used by adipose tissue, liver, and skeletal and cardiac muscle as a primary energy source
Copyright © 2010 Pearson Education, Inc. Absorptive State Proteins Excess amino acids are deaminated and used for ATP synthesis or stored as fat in the liver Most amino acids are used in protein synthesis
Copyright © 2010 Pearson Education, Inc. Figure 24.19a (a) Major events of the absorptive state Major energy fuel: glucose (dietary) Liver metabolism: amino acids deaminated and used for energy or stored as fat Major metabolic thrust: anabolism and energy storage Amino acids Proteins Glycogen Glucose Amino acids Keto acids Fats CO 2 + H 2 O + Triglycerides Glycerol and fatty acids CO 2 + H 2 O +
Copyright © 2010 Pearson Education, Inc. Figure 24.19b (b) Principal pathways of the absorptive state Amino acids Protein Keto acids Fats Glucose Glycogen Protein Glucose Gastrointestinal tract In liver: In all tissues: In adipose tissue: Glucose Fatty acids Fatty acids Glyceraldehyde- phosphate Glycerol Fatty acids In muscle: CO 2 + H 2 O + +
Copyright © 2010 Pearson Education, Inc. Absorptive State: Hormonal Control Insulin secretion is stimulated by Elevated blood levels of glucose and amino acids GIP and parasympathetic stimulation
Copyright © 2010 Pearson Education, Inc. Insulin Effects on Metabolism Insulin, a hypoglycemic hormone, enhances Facilitated diffusion of glucose into muscle and adipose cells Glucose oxidation Glycogen and triglyceride formation Active transport of amino acids into tissue cells Protein synthesis
Copyright © 2010 Pearson Education, Inc. Figure Stimulates Targets tissue cells Beta cells of pancreatic islets Blood glucose Blood insulin Active transport of amino acids into tissue cells Facilitated diffusion of glucose into tissue cells Protein synthesis Cellular respiration Enhances glucose conversion to: CO 2 + H 2 O + Fatty acids + glycerol Glycogen Initial stimulus Physiological response Result
Copyright © 2010 Pearson Education, Inc. Postabsorptive State Catabolism of fat, glycogen, and proteins exceeds anabolism Goal is to maintain blood glucose between meals Makes glucose available to the blood Promotes use of fats for energy (glucose sparing)
Copyright © 2010 Pearson Education, Inc. Sources of Blood Glucose 1.Glycogenolysis in the liver 2.Glycogenolysis in skeletal muscle 3.Lipolysis in adipose tissues and the liver Glycerol is used for gluconeogenesis in the liver
Copyright © 2010 Pearson Education, Inc. Sources of Blood Glucose 4.Catabolism of cellular protein during prolonged fasting Amino acids are deaminated and used for gluconeogenesis in the liver and (later) in the kidneys
Copyright © 2010 Pearson Education, Inc. Figure 24.21a (a) Major events of the postabsorptive state Major energy fuels: glucose provided by glycogenolysis and gluconeogenesis, fatty acids, and ketones Liver metabolism: amino acids converted to glucose Major metabolic thrust: catabolism and replacement of fuels in blood Amino acids ProteinsGlycogen Glucose Fatty acids and ketones Glucose Amino acids Keto acids Glucose Triglycerides Glycerol and fatty acids CO 2 + H 2 O +
Copyright © 2010 Pearson Education, Inc. Figure 24.21b (b) Principal pathways of the postabsorptive state Amino acids Fatty acids Glycerol Fatty acids + glycerol Ketone bodies Blood glucoseGlucose Keto acids Keto acids Stored glycogen Glycogen Protein Pyruvic and lactic acids Fat Pyruvic and lactic acids In nervous tissue: In liver: In most tissues: In adipose tissue: In muscle: CO 2 + H 2 O
Copyright © 2010 Pearson Education, Inc. Postabsorptive State: Hormonal Controls Glucagon release is stimulated by Declining blood glucose Rising amino acid levels
Copyright © 2010 Pearson Education, Inc. Effects of Glucagon Glucagon, a hyperglycemic hormone, promotes Glycogenolysis and gluconeogenesis in the liver Lipolysis in adipose tissue Modulation of glucose effects after a high- protein, low-carbohydrate meal
Copyright © 2010 Pearson Education, Inc. Figure Plasma glucose (and rising amino acid levels) Stimulates Plasma glucagon Plasma fatty acids Liver Alpha cells of pancreatic islets Stimulates glycogenolysis and gluconeogenesis Negative feedback: rising glucose levels shut off initial stimulus Stimulates fat breakdown Reduces, inhibits Increases, stimulates Adipose tissue Initial stimulus Physiological response Result Fat used by tissue cells = glucose sparing Plasma glucose (and insulin)
Copyright © 2010 Pearson Education, Inc. Postabsorptive State: Neural Controls In response to low plasma glucose, or during fight-or-flight or exercise, the sympathetic nervous system and epinephrine from the adrenal medulla promote Fat mobilization Glycogenolysis
Copyright © 2010 Pearson Education, Inc. Metabolic Role of the Liver Hepatocytes Process nearly every class of nutrient Play a major role in regulating plasma cholesterol levels Store vitamins and minerals Metabolize alcohol, drugs, hormones, and bilirubin
Copyright © 2010 Pearson Education, Inc. Cholesterol Structural basis of bile salts, steroid hormones, and vitamin D Major component of plasma membranes Makes up part of the hedgehog signaling molecule that directs embryonic development Transported in lipoprotein complexes containing triglycerides, phospholipids, cholesterol, and protein
Copyright © 2010 Pearson Education, Inc. Lipoproteins Types of lipoproteins HDLs (high-density lipoproteins) The highest protein content LDLs (low-density lipoproteins) Cholesterol-rich VLDLs (very low density lipoproteins) Mostly triglycerides Chylomicrons
Copyright © 2010 Pearson Education, Inc. Figure Triglyceride Phospholipid Cholesterol Protein 2–7% 1–2% ChylomicronVLDLLDLHDL 3–6% 80–95% 55–65% 10% 5% 20% 30% 20% 45–50% 45% 25% 10–15% 5–10% 15–20% From intestineMade by liverReturned to liver
Copyright © 2010 Pearson Education, Inc. Lipoproteins VLDLs Transport triglycerides to peripheral tissues (mostly adipose) LDLs Transport cholesterol to peripheral tissues for membranes, storage, or hormone synthesis HDLs Transport excess cholesterol from peripheral tissues to the liver to be broken down and secreted into bile Also provide cholesterol to steroid-producing organs
Copyright © 2010 Pearson Education, Inc. Lipoproteins High levels of HDL are thought to protect against heart attack High levels of LDL, especially lipoprotein (a) increase the risk of heart attack
Copyright © 2010 Pearson Education, Inc. Plasma Cholesterol Levels The liver produces cholesterol At a basal level regardless of dietary cholesterol intake In response to saturated fatty acids
Copyright © 2010 Pearson Education, Inc. Plasma Cholesterol Levels Saturated fatty acids Stimulate liver synthesis of cholesterol Inhibit cholesterol excretion from the body Unsaturated fatty acids Enhance excretion of cholesterol
Copyright © 2010 Pearson Education, Inc. Plasma Cholesterol Levels Trans fats Increase LDLs and reduce HDLs
Copyright © 2010 Pearson Education, Inc. Plasma Cholesterol Levels Unsaturated omega-3 fatty acids (found in cold-water fish) Lower the proportions of saturated fats and cholesterol Have antiarrhythmic effects on the heart Help prevent spontaneous clotting Lower blood pressure
Copyright © 2010 Pearson Education, Inc. Non-Dietary Factors Affecting Cholesterol Stress, cigarette smoking, and coffee lower HDL levels Aerobic exercise and estrogen increase HDL levels and decrease LDL levels Body shape “Apple”: Fat carried on the upper body is correlated with high cholesterol and LDL levels “Pear”: Fat carried on the hips and thighs is correlated with lower cholesterol and LDL levels
Copyright © 2010 Pearson Education, Inc. Energy Balance Bond energy released from food must equal the total energy output Energy intake = the energy liberated during food oxidation Energy output Immediately lost as heat (~60%) Used to do work (driven by ATP) Stored as fat or glycogen
Copyright © 2010 Pearson Education, Inc. Energy Balance Heat energy Cannot be used to do work Warms the tissues and blood Helps maintain the homeostatic body temperature Allows metabolic reactions to occur efficiently
Copyright © 2010 Pearson Education, Inc. Obesity Body mass index (BMI) = wt (lb) 705/ht (inches) 2 Considered overweight if BMI is 25 to 30 Considered obese if BMI is greater than 30 Higher incidence of atherosclerosis, diabetes mellitus, hypertension, heart disease, and osteoarthritis
Copyright © 2010 Pearson Education, Inc. Regulation of Food Intake Two distinct sets of hypothalamic neurons 1.LHA neurons promote hunger when stimulated by neuropeptides (e.g., NPY) 2.VMN neurons cause satiety through release of CRH when stimulated by appetite- suppressing peptides (e.g., POMC and CART peptides)
Copyright © 2010 Pearson Education, Inc. Regulation of Food Intake Factors that affect brain thermoreceptors and chemoreceptors Neural signals from the digestive tract Bloodborne signals related to body energy stores Hormones To a lesser extent, body temperature and psychological factors
Copyright © 2010 Pearson Education, Inc. Short-Term Regulation of Food Intake Neural signals High protein content of meal increases and prolongs afferent vagal signals Distension sends signals along the vagus nerve that suppress the hunger center
Copyright © 2010 Pearson Education, Inc. Short-Term Regulation of Food Intake Nutrient signals Increased nutrient levels in the blood depress eating Blood glucose Amino acids Fatty acids
Copyright © 2010 Pearson Education, Inc. Short-Term Regulation of Food Intake Hormones Gut hormones (e.g., insulin and CCK) depress hunger Glucagon and epinephrine stimulate hunger Ghrelin (Ghr) from the stomach stimulates appetite just before a meal
Copyright © 2010 Pearson Education, Inc. Long-Term Regulation of Food Intake Leptin Hormone secreted by fat cells in response to increased body fat mass Indicator of total energy stores in fat tissue Protects against weight loss in times of nutritional deprivation
Copyright © 2010 Pearson Education, Inc. Long-Term Regulation of Food Intake Leptin Acts on the ARC neurons in the hypothalamus Suppresses the secretion of NPY, a potent appetite stimulant Stimulates the expression of appetite suppressants (e.g., CART peptides)
Copyright © 2010 Pearson Education, Inc. Figure Long-term controlsShort-term controls Hunger (appetite enhancement) LHA (orexin- releasing neurons) Satiety (appetite suppression) VMN (CRH- releasing neurons) Release orexins Release CRH Release melano- cortins Release NPY ARC nucleus NPY/ AgRP group POMC/ CART group Insulin (from pancreas) Leptin (from lipid storage) Solitary nucleus Stretch (distension of GI tract) Glucose Amino acids Fatty acids Ghrelin Glucagon Epinephrine Gut hormones and others Stimulates Inhibits Insulin PYY CCK Gut hormones Nutrient signals Vagal afferents HypothalamusBrain stem
Copyright © 2010 Pearson Education, Inc. Long-Term Regulation of Food Intake Additional factors Temperature Stress Psychological factors Adenovirus infections Sleep deprivation
Copyright © 2010 Pearson Education, Inc. Metabolic Rate Total heat produced by chemical reactions and mechanical work of the body Measured directly with a calorimeter or indirectly with a respirometer
Copyright © 2010 Pearson Education, Inc. Metabolic Rate Basal metabolic rate (BMR) Reflects the energy the body needs to perform its most essential activities
Copyright © 2010 Pearson Education, Inc. Factors that Influence BMR As the ratio of body surface area to volume increases, BMR increases Decreases with age Increases with temperature or stress Males have a disproportionately higher BMR Thyroxine increases oxygen consumption, cellular respiration, and BMR
Copyright © 2010 Pearson Education, Inc. Metabolic Rate Total metabolic rate (TMR) Rate of kilocalorie consumption to fuel all ongoing activities Increases with skeletal muscle activity and food ingestion
Copyright © 2010 Pearson Education, Inc. Regulation of Body Temperature Body temperature reflects the balance between heat production and heat loss At rest, the liver, heart, brain, kidneys, and endocrine organs generate most heat During exercise, heat production from skeletal muscles increases dramatically
Copyright © 2010 Pearson Education, Inc. Regulation of Body Temperature Normal body temperature = 37 C 5 C (98.6 F) Optimal enzyme activity occurs at this temperature Increased temperature denatures proteins and depresses neurons
Copyright © 2010 Pearson Education, Inc. Figure Basal metabolism Muscular activity (shivering) Thyroxine and epinephrine (stimulating effects on metabolic rate) Temperature effect on cells Radiation Conduction/ convection Evaporation Heat productionHeat loss
Copyright © 2010 Pearson Education, Inc. Core and Shell Temperature Organs in the core have the highest temperature Blood is the major agent of heat exchange between the core and the shell Core temperature is regulated Core temperature remains relatively constant, while shell temperature fluctuates substantially (20 C–40 C)
Copyright © 2010 Pearson Education, Inc. Mechanisms of Heat Exchange Four mechanisms 1.Radiation is the loss of heat in the form of infrared rays 2.Conduction is the transfer of heat by direct contact 3.Convection is the transfer of heat to the surrounding air 4.Evaporation is the heat loss due to the evaporation of water from body surfaces
Copyright © 2010 Pearson Education, Inc. Figure 24.26
Copyright © 2010 Pearson Education, Inc. Mechanisms of Heat Exchange Insensible heat loss accompanies insensible water loss from lungs, oral mucosa, and skin Evaporative heat loss becomes sensible (active) when body temperature rises and sweating increases water vaporization
Copyright © 2010 Pearson Education, Inc. Role of the Hypothalamus Preoptic region of the hypothalamus contains the two thermoregulatory centers Heat-loss center Heat-promoting center
Copyright © 2010 Pearson Education, Inc. Role of the Hypothalamus The hypothalamus receives afferent input from Peripheral thermoreceptors in the skin Central thermoreceptors (some in the hypothalamus) Initiates appropriate heat-loss and heat- promoting activities
Copyright © 2010 Pearson Education, Inc. Heat-Promoting Mechanisms Constriction of cutaneous blood vessels Shivering Increased metabolic rate via epinephrine and norepinephrine Enhanced thyroxine release
Copyright © 2010 Pearson Education, Inc. Heat-Promoting Mechanisms Voluntary measures include Putting on more clothing Drinking hot fluids Changing posture or increasing physical activity
Copyright © 2010 Pearson Education, Inc. Heat-Loss Mechanisms Dilation of cutaneous blood vessels Enhanced sweating Voluntary measures include Reducing activity and seeking a cooler environment Wearing light-colored and loose-fitting clothing
Copyright © 2010 Pearson Education, Inc. Figure 24.27, step 1 Activates heat- loss center in hypothalamus Sweat glands activated: secrete perspiration, which is vaporized by body heat, helping to cool the body Skin blood vessels dilate: capillaries become flushed with warm blood; heat radiates from skin surface Body temperature decreases: blood temperature declines and hypothalamus heat-loss center “shuts off” Stimulus Increased body temperature; blood warmer than hypothalamic set point
Copyright © 2010 Pearson Education, Inc. Figure 24.27, step 2 Stimulus Decreased body tempera- ture; blood cooler than hypothalamic set point Body temperature increases: blood temperature rises and hypothalamus heat-promoting center “shuts off” Activates heat- promoting center in hypothalamus Skeletal muscles activated when more heat must be generated; shivering begins Skin blood vessels constrict: blood is diverted from skin capillaries and withdrawn to deeper tissues; minimizes overall heat loss from skin surface
Copyright © 2010 Pearson Education, Inc. Homeostatic Imbalance Hyperthermia Elevated body temperature depresses the hypothalamus Positive-feedback mechanism (heat stroke) begins at core temperature of 41 C Can be fatal if not corrected
Copyright © 2010 Pearson Education, Inc. Homeostatic Imbalance Heat exhaustion Heat-associated collapse after vigorous exercise Due to dehydration and low blood pressure Heat-loss mechanisms are still functional May progress to heat stroke
Copyright © 2010 Pearson Education, Inc. Homeostatic Imbalance Hypothermia Low body temperature where vital signs decrease Shivering stops at core temperature of C Can progress to coma a death by cardiac arrest at ~ 21 C
Copyright © 2010 Pearson Education, Inc. Fever Controlled hyperthermia Due to infection (also cancer, allergies, or CNS injuries) Macrophages release interleukins (“pyrogens”) that cause the release of prostaglandins from the hypothalamus
Copyright © 2010 Pearson Education, Inc. Fever Prostaglandins reset the hypothalamic thermostat higher Natural body defenses or antibiotics reverse the disease process; cryogens (e.g., vasopressin) reset the thermostat to a lower (normal) level
Copyright © 2010 Pearson Education, Inc. Developmental Aspects Lack of proteins in utero and in the first three years mental deficits and learning disorders Insulin-dependent diabetes mellitus and genetic disorders metabolic problems in children Non-insulin–dependent diabetes mellitus may occur in middle and old age, especially in obese people Metabolic rate declines throughout the life span
Copyright © 2010 Pearson Education, Inc. Developmental Aspects Many medications for age-related problems influence nutrition: Diuretics for heart failure and hypertension increase the risk of hypokalemia Some antibiotics interfere with digestion and absorption Mineral oil (laxative) decrease absorption of fat-soluble vitamins Excessive alcohol consumption may lead to malabsorption, vitamin and mineral deficiencies, deranged metabolism, damage to liver and pancreas
Copyright © 2010 Pearson Education, Inc. Developmental Aspects Nonenzymatic binding of glucose to proteins increases with age, leading to lens clouding and general tissue stiffening
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