Nutrition, Metabolism, and Body Temperature Regulation 24 P A R T B Nutrition, Metabolism, and Body Temperature Regulation
Oxidation of Amino Acids Transamination – switching of an amine group from an amino acid to a keto acid (usually -ketoglutaric acid of the Krebs cycle) Typically, glutamic acid is formed in this process
Oxidation of Amino Acids Oxidative deamination – the amine group of glutamic acid is: Released as ammonia Combined with carbon dioxide in the liver Excreted as urea by the kidneys Keto acid modification – keto acids from transamination are altered to produce metabolites that can enter the Krebs cycle
Amino acids are the most important anabolic nutrients, and they form: Synthesis of Proteins Amino acids are the most important anabolic nutrients, and they form: All protein structures The bulk of the body’s functional molecules
Amounts and types of proteins: Synthesis of Proteins Amounts and types of proteins: Are hormonally controlled Reflect each life cycle stage A complete set of amino acids is necessary for protein synthesis All essential amino acids must be provided in the diet
Summary: Carbohydrate Metabolic Reactions Table 24.4.1
Summary: Lipid and Protein Metabolic Reactions Table 24.4.2
State of the Body The body exists in a dynamic catabolic-anabolic state Organic molecules (except DNA) are continuously broken down and rebuilt The body’s total supply of nutrients constitutes its nutrient pool
State of the Body Amino acid pool – body’s total supply of free amino acids is the source for: Resynthesizing body proteins Forming amino acid derivatives Gluconeogenesis
Carbohydrate/Fat and Amino Acid Pools Figure 24.16
Interconversion Pathways of Nutrients Carbohydrates are easily and frequently converted into fats Their pools are linked by key intermediates They differ from the amino acid pool in that: Fats and carbohydrates are oxidized directly to produce energy Excess carbohydrate and fat can be stored
Interconversion Pathways of Nutrients Figure 24.17
Absoprtive and Postabsorptive States Metabolic controls equalize blood concentrations of nutrients between two states Absorptive The time during and shortly after nutrient intake Postabsorptive The time when the GI tract is empty Energy sources are supplied by the breakdown of body reserves
The major metabolic thrust is anabolism and energy storage Absoprtive State The major metabolic thrust is anabolism and energy storage Amino acids become proteins Glycerol and fatty acids are converted to triglycerides Glucose is stored as glycogen Dietary glucose is the major energy fuel Excess amino acids are deaminated and used for energy or stored as fat in the liver
Absoprtive State Figure 24.18a
Principal Pathways of the Absorptive State In muscle: Amino acids become protein Glucose is converted to glycogen In the liver: Amino acids become protein or are deaminated to keto acids Glucose is stored as glycogen or converted to fat
Principal Pathways of the Absorptive State In adipose tissue: Glucose and fats are converted and stored as fat All tissues use glucose to synthesize ATP
Principal Pathways of the Absorptive State Figure 24.18b
Insulin Effects on Metabolism Insulin controls the absorptive state and its secretion is stimulated by: Increased blood glucose Elevated amino acid levels in the blood Gastrin, CCK, and secretin
Insulin Effects on Metabolism Insulin enhances: Active transport of amino acids into tissue cells Facilitated diffusion of glucose into tissue
Insulin Effects on Metabolism Figure 24.19
Diabetes Mellitus A consequence of inadequate insulin production or abnormal insulin receptors Glucose becomes unavailable to most body cells Metabolic acidosis, protein wasting, and weight loss result as fats and tissue proteins are used for energy
Glucose is provided by glycogenolysis and gluconeogenesis Postabsorptive State The major metabolic thrust is catabolism and replacement of fuels in the blood Proteins are broken down to amino acids Triglycerides are turned into glycerol and fatty acids Glycogen becomes glucose Glucose is provided by glycogenolysis and gluconeogenesis Fatty acids and ketones are the major energy fuels Amino acids are converted to glucose in the liver
Postabsorptive State Figure 24.20a
Principle Pathways in the Postabsorptive State In muscle: Protein is broken down to amino acids Glycogen is converted to ATP and pyruvic acid (lactic acid in anaerobic states)
Principle Pathways in the Postabsorptive State In the liver: Amino acids, pyruvic acid, stored glycogen, and fat are converted into glucose Fat is converted into keto acids that are used to make ATP Fatty acids (from adipose tissue) and ketone bodies (from the liver) are used in most tissue to make ATP Glucose from the liver is used by the nervous system to generate ATP
Principle Pathways in the Postabsorptive State Figure 24.20b
Hormonal and Neural Controls of the Postabsorptive State Decreased plasma glucose concentration and rising amino acid levels stimulate alpha cells of the pancreas to secrete glucagon (the antagonist of insulin) Glucagon stimulates: Glycogenolysis and gluconeogenesis Fat breakdown in adipose tissue Glucose sparing
Influence of Glucagon Figure 24.21
Hormonal and Neural Controls of the Postabsorptive State In response to low plasma glucose, the sympathetic nervous system releases epinephrine, which acts on the liver, skeletal muscle, and adipose tissue to mobilize fat and promote glycogenolysis
Liver Metabolism Hepatocytes carry out over 500 intricate metabolic functions
A brief summary of liver functions Liver Metabolism A brief summary of liver functions Packages fatty acids to be stored and transported Synthesizes plasma proteins Forms nonessential amino acids Converts ammonia from deamination to urea Stores glucose as glycogen, and regulates blood glucose homeostasis Stores vitamins, conserves iron, degrades hormones, and detoxifies substances
Cholesterol Is the structural basis of bile salts, steroid hormones, and vitamin D Makes up part of the hedgehog molecule that directs embryonic development Is transported to and from tissues via lipoproteins
Lipoproteins are classified as: Cholesterol Lipoproteins are classified as: HDLs – high-density lipoproteins have more protein content LDLs – low-density lipoproteins have a considerable cholesterol component VLDLs – very low density lipoproteins are mostly triglycerides
Cholesterol Figure 24.22
HDLs transport excess cholesterol from peripheral tissues to the liver Lipoproteins The liver is the main source of VLDLs, which transport triglycerides to peripheral tissues (especially adipose) LDLs transport cholesterol to the peripheral tissues and regulate cholesterol synthesis HDLs transport excess cholesterol from peripheral tissues to the liver Also serve the needs of steroid-producing organs (ovaries and adrenal glands)
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
Plasma Cholesterol Levels The liver produces cholesterol: At a basal level of cholesterol regardless of dietary intake Via a negative feedback loop involving serum cholesterol levels In response to saturated fatty acids
Plasma Cholesterol Levels Fatty acids regulate excretion of cholesterol Unsaturated fatty acids enhance excretion Saturated fatty acids inhibit excretion Certain unsaturated fatty acids (omega-3 fatty acids, found in cold-water fish) lower the proportions of saturated fats and cholesterol
Non-Dietary Factors Affecting Cholesterol Stress, cigarette smoking, and coffee drinking increase LDL levels Aerobic exercise increases HDL levels Body shape is correlated with cholesterol levels Fat carried on the upper body is correlated with high cholesterol levels Fat carried on the hips and thighs is correlated with lower levels
Energy output includes the energy: Body Energy Balance Bond energy released from catabolized food must equal the total energy output Energy intake – equal to the energy liberated during the oxidation of food Energy output includes the energy: Immediately lost as heat (about 60% of the total) Used to do work (driven by ATP) Stored in the form of fat and glycogen
Nearly all energy derived from food is eventually converted to heat Body Energy Balance Nearly all energy derived from food is eventually converted to heat Cells cannot use this energy to do work, but the heat: Warms the tissues and blood Helps maintain the homeostatic body temperature Allows metabolic reactions to occur efficiently
Regulation of Food Intake When energy intake and energy outflow are balanced, body weight remains stable The hypothalamus releases peptides that influence feeding behavior Orexins are powerful appetite enhancers Neuropeptide Y causes a craving for carbohydrates Galanin produces a craving for fats GLP-1 and serotonin make us feel full and satisfied
Feeding behavior and hunger depend on one or more of five factors Feeding Behaviors Feeding behavior and hunger depend on one or more of five factors Neural signals from the digestive tract Bloodborne signals related to the body energy stores Hormones, body temperature, and psychological factors
Nutrient Signals Related to Energy Stores High plasma levels of nutrients that signal depressed eating Plasma glucose levels Amino acids in the plasma Fatty acids and leptin
Hormones, Temperature, and Psychological Factors Glucagon and epinephrine stimulate hunger Insulin and cholecystokinin depress hunger Increased body temperature may inhibit eating behavior Psychological factors that have little to do with caloric balance can also influence eating behaviors
Control of Feeding Behavior and Satiety Leptin, secreted by fat tissue, appears to be the overall satiety signal Acts on the ventromedial hypothalamus Controls appetite and energy output Suppresses the secretion of neuropeptide Y, a potent appetite stimulant Blood levels of insulin and glucocorticoids play a role in regulating leptin release
Hypothalamic Command of Appetite Figure 24.23
Measured directly with a calorimeter or indirectly with a respirometer Metabolic Rate Rate of energy output (expressed per hour) equal to the total heat produced by: All the chemical reactions in the body The mechanical work of the body Measured directly with a calorimeter or indirectly with a respirometer
Basal metabolic rate (BMR) Reflects the energy the body needs to perform its most essential activities Total metabolic rate (TMR) Total rate of kilocalorie consumption to fuel all ongoing activities
Factors that Influence BMR Surface area, age, gender, stress, and hormones As the ratio of surface area to volume increases, BMR increases Males have a disproportionately high BMR Stress increases BMR Thyroxine increases oxygen consumption, cellular respiration, and BMR
Regulation of Body Temperature Body temperature – balance between heat production and heat loss At rest, the liver, heart, brain, and endocrine organs account for most heat production During vigorous exercise, heat production from skeletal muscles can increase 30–40 times
Regulation of Body Temperature Normal body temperature is 36.2C (98.2F); optimal enzyme activity occurs at this temperature Temperature spikes above this range denature proteins and depress neurons
Regulation of Body Temperature Figure 24.24
Core and Shell Temperature Organs in the core (within the skull, thoracic, and abdominal cavities) have the highest temperature The shell, essentially the skin, has the lowest temperature Blood serves as the major agent of heat transfer between the core and shell Core temperature remains relatively constant, while shell temperature fluctuates substantially (20C–40C)
Mechanisms of Heat Exchange Four mechanisms: Radiation – loss of heat in the form of infrared rays Conduction – transfer of heat by direct contact Convection – transfer of heat to the surrounding air Evaporation – heat loss due to the evaporation of water from the lungs, mouth mucosa, and skin (insensible heat loss) Evaporative heat loss becomes sensible when body temperature rises and sweating produces increased water for vaporization
Role of the Hypothalamus The main thermoregulation center is the preoptic region of the hypothalamus The heat-loss and heat-promoting centers comprise the thermoregulatory centers The hypothalamus: Receives input from thermoreceptors in the skin and core Responds by initiating appropriate heat-loss and heat-promoting activities
Heat-Promoting Mechanisms Low external temperature or low temperature of circulating blood activates heat-promoting centers of the hypothalamus to cause: Vasoconstriction of cutaneous blood vessels Increased metabolic rate Shivering Enhanced thyroxine release
Voluntary measures commonly taken to reduce body heat include: Heat-Loss Mechanisms When the core temperature rises, the heat-loss center is activated to cause: Vasodilation of cutaneous blood vessels Enhanced sweating Voluntary measures commonly taken to reduce body heat include: Reducing activity and seeking a cooler environment Wearing light-colored and loose-fitting clothing
Figure 24.26 Skin blood vessels dilate: capillaries become flushed with warm blood; heat radiates from skin surface Activates heat-loss center in hypothalamus Body temper- ature decreases: blood temperature declines and hypo- thalamus heat-loss center “shuts off” Sweat glands activated: secrete perspiration, which is vaporized by body heat, helping to cool the body Blood warmer than hypothalamic set point Stimulus: Increased body temperature (e.g., when exercising or the climate is hot) Imbalance Stimulus: Decreased body temperature (e.g., due to cold environmental temperatures) Homeostasis = normal body temperature (35.8°C–38.2°C) Imbalance Blood cooler than hypothalamic set point Skin blood vessels constrict: blood is diverted from skin capillaries and withdrawn to deeper tissues; minimizes overall heat loss from skin surface Body temper- ature increases: blood temperature rises and hypothala- mus heat-promoting center “shuts off” Activates heat- promoting center in hypothalamus Skeletal muscles activated when more heat must be generated; shivering begins Figure 24.26
Homeostasis = normal body temperature (35.8°C–38.2°C) Stimulus: Increased body temperature (e.g., when exercising or the climate is hot) Imbalance Homeostasis = normal body temperature (35.8°C–38.2°C) Imbalance Figure 24.26
Homeostasis = normal body temperature (35.8°C–38.2°C) Activates heat-loss center in hypothalamus Blood warmer than hypothalamic set point Stimulus: Increased body temperature (e.g., when exercising or the climate is hot) Imbalance Homeostasis = normal body temperature (35.8°C–38.2°C) Imbalance Figure 24.26
radiates from skin surface Activates heat-loss center in hypothalamus Skin blood vessels dilate: capillaries become flushed with warm blood; heat radiates from skin surface Activates heat-loss center in hypothalamus Blood warmer than hypothalamic set point Stimulus: Increased body temperature (e.g., when exercising or the climate is hot) Imbalance Homeostasis = normal body temperature (35.8°C–38.2°C) Imbalance Figure 24.26
radiates from skin surface Activates heat-loss center in hypothalamus Skin blood vessels dilate: capillaries become flushed with warm blood; heat radiates from skin surface Activates heat-loss center in hypothalamus Sweat glands activated: secrete perspiration, which is vaporized by body heat, helping to cool the body Body temper- ature decreases: blood temperature declines and hypo- thalamus heat-loss center “shuts off” Blood warmer than hypothalamic set point Stimulus: Increased body temperature (e.g., when exercising or the climate is hot) Imbalance Homeostasis = normal body temperature (35.8°C–38.2°C) Imbalance Figure 24.26
radiates from skin surface Activates heat-loss center in hypothalamus Skin blood vessels dilate: capillaries become flushed with warm blood; heat radiates from skin surface Activates heat-loss center in hypothalamus Sweat glands activated: secrete perspiration, which is vaporized by body heat, helping to cool the body Body temper- ature decreases: blood temperature declines and hypo- thalamus heat-loss center “shuts off” Blood warmer than hypothalamic set point Stimulus: Increased body temperature (e.g., when exercising or the climate is hot) Homeostasis = normal body temperature (35.8°C–38.2°C) Figure 24.26
Homeostasis = normal body temperature (35.8°C–38.2°C) Imbalance Stimulus: Decreased body temperature (e.g., due to cold environmental temperatures) Homeostasis = normal body temperature (35.8°C–38.2°C) Imbalance Figure 24.26
Homeostasis = normal body temperature (35.8°C–38.2°C) Imbalance Stimulus: Decreased body temperature (e.g., due to cold environmental temperatures) Homeostasis = normal body temperature (35.8°C–38.2°C) Imbalance Blood cooler than hypothalamic set point Activates heat- promoting center in hypothalamus Figure 24.26
Homeostasis = normal body temperature (35.8°C–38.2°C) Imbalance Stimulus: Decreased body temperature (e.g., due to cold environmental temperatures) Homeostasis = normal body temperature (35.8°C–38.2°C) Imbalance Blood cooler than hypothalamic set point Activates heat- promoting center in hypothalamus Skeletal muscles activated when more heat must be generated; shivering begins Figure 24.26
Homeostasis = normal body temperature (35.8°C–38.2°C) Imbalance Stimulus: Decreased body temperature (e.g., due to cold environmental temperatures) Homeostasis = normal body temperature (35.8°C–38.2°C) Imbalance Blood cooler than hypothalamic set point Skin blood vessels constrict: blood is diverted from skin capillaries and withdrawn to deeper tissues; minimizes overall heat loss from skin surface Activates heat- promoting center in hypothalamus Skeletal muscles activated when more heat must be generated; shivering begins Figure 24.26
Homeostasis = normal body temperature (35.8°C–38.2°C) Imbalance Stimulus: Decreased body temperature (e.g., due to cold environmental temperatures) Homeostasis = normal body temperature (35.8°C–38.2°C) Imbalance Blood cooler than hypothalamic set point Skin blood vessels constrict: blood is diverted from skin capillaries and withdrawn to deeper tissues; minimizes overall heat loss from skin surface Body temper- ature increases: blood temperature rises and hypothala- mus heat-promoting center “shuts off” Activates heat- promoting center in hypothalamus Skeletal muscles activated when more heat must be generated; shivering begins Figure 24.26
Homeostasis = normal body temperature (35.8°C–38.2°C) Stimulus: Decreased body temperature (e.g., due to cold environmental temperatures) Homeostasis = normal body temperature (35.8°C–38.2°C) Blood cooler than hypothalamic set point Skin blood vessels constrict: blood is diverted from skin capillaries and withdrawn to deeper tissues; minimizes overall heat loss from skin surface Body temper- ature increases: blood temperature rises and hypothala- mus heat-promoting center “shuts off” Activates heat- promoting center in hypothalamus Skeletal muscles activated when more heat must be generated; shivering begins Figure 24.26
Figure 24.26 Skin blood vessels dilate: capillaries become flushed with warm blood; heat radiates from skin surface Activates heat-loss center in hypothalamus Body temper- ature decreases: blood temperature declines and hypo- thalamus heat-loss center “shuts off” Sweat glands activated: secrete perspiration, which is vaporized by body heat, helping to cool the body Blood warmer than hypothalamic set point Stimulus: Increased body temperature (e.g., when exercising or the climate is hot) Imbalance Stimulus: Decreased body temperature (e.g., due to cold environmental temperatures) Homeostasis = normal body temperature (35.8°C–38.2°C) Imbalance Blood cooler than hypothalamic set point Skin blood vessels constrict: blood is diverted from skin capillaries and withdrawn to deeper tissues; minimizes overall heat loss from skin surface Body temper- ature increases: blood temperature rises and hypothala- mus heat-promoting center “shuts off” Activates heat- promoting center in hypothalamus Skeletal muscles activated when more heat must be generated; shivering begins Figure 24.26
Hyperthermia Normal heat loss processes become ineffective and elevated body temperatures depress the hypothalamus This sets up a positive-feedback mechanism, sharply increasing body temperature and metabolic rate This condition, called heat stroke, can be fatal if not corrected
Heat Exhaustion Heat-associated collapse after vigorous exercise, evidenced by elevated body temperature, mental confusion, and fainting Due to dehydration and low blood pressure Heat-loss mechanisms are fully functional Can progress to heat stroke if the body is not cooled and rehydrated
Fever Controlled hyperthermia, often a result of infection, cancer, allergic reactions, or central nervous system injuries White blood cells, injured tissue cells, and macrophages release pyrogens that act on the hypothalamus, causing the release of prostaglandins Prostaglandins reset the hypothalamic thermostat The higher set point is maintained until the natural body defenses reverse the disease process
Developmental Aspects Good nutrition is essential in utero as well as throughout life Lack of proteins needed for fetal growth and in the first three years of life can lead to mental deficits and learning disorders With the exception of insulin-dependent diabetes mellitus, children free of genetic disorders rarely exhibit metabolic problems In later years, non-insulin-dependent diabetes mellitus becomes a major problem
Developmental Aspects Many agents prescribed for age-related medical problems influence nutrition Diuretics can cause hypokalemia by promoting potassium loss Antibiotics can interfere with food absorption Mineral oil interferes with absorption of fat-soluble vitamins Excessive alcohol consumption leads to malabsorption problems, certain vitamin and mineral deficiencies, deranged metabolism, and damage to the liver and pancreas