PowerPoint Lecture Outline Chapter 12: Ingestive Behavior: Eating Carlson-Physiology of Behavior 6/e, Allyn and Bacon Eating The primary function of eating is to obtain and to store energy Food contains carbohydrates, fat, protein, minerals Digestion breaks down ingested nutrients and stores as energy Glycogen (short-term) Triglyceride (long-term) Eating behaviors Appetitive: behaviors that locate food Consummatory: behaviors that place food in the gut for absorption Biting, chewing Sucking Swallowing 13.* Carlson-Physiology of Behavior 6/e, Allyn and Bacon The Fasting and Absorptive Phases of Metabolism 13.* Insulin (parasymp.) Glucagon (sympath.) Carlson-Physiology of Behavior 6/e, Allyn and Bacon Eating Initiation The factors that start a meal are distinct from those that terminate a meal Environmental factors can start a meal Habit Meal schedule dictates the intermeal interval We are able to adjust meal size, not intermeal interval Conditioned environmental cues (conditioned eating) Stimuli in the environment A clock (breakfast at 8 am, lunch at noon, dinner at 6 pm) The sight/smell of food Presence of other persons Meal size goes up with group size 13.* Carlson-Physiology of Behavior 6/e, Allyn and Bacon Short-Term Hunger Signals Glucoprivation is a decline in glucose available to cells ? leads to hunger 2-DG induces glucoprivation by competing with glucose for metabolism and transport into the cell D-DG stimulates eating Lipoprivation refers to a lack of fatty acids available to cells Methyl palmoxirate (MP) and mercaptoacetate (MA) induce lipoprivation by interfering with the metabolism of fatty acids 13.* Carlson-Physiology of Behavior 6/e, Allyn and Bacon Impairment of Glucose and Lipid Metabolism Stimulates Eating 13.* Glucoprivation Lipoprivation Combination of 2-DG and MP is sufficient to stimulate eating Carlson-Physiology of Behavior 6/e, Allyn and Bacon Glucoreceptors in Liver and Brain Liver (may respond to both gluco- and lipoprivic signals) Liver contains glucoreceptors that report to brain via vagus nerve Infusions of 2-DG into hepatic portal vein produce immediate eating Transection of the vagus prevents the stimulatory effect of 2-DG on eating 2,5-AM blocks glucose metabolism (like 2-DG) AND increases firing rate in the vagus (which reports to the brain) Brain (uses only glucose for fuel) Infusions of 5-TG into fourth ventricle block glucose metabolism and induce eating Infusion of glucose into the ventricles prevented eating produced by systemic 2-DG 13.* Carlson-Physiology of Behavior 6/e, Allyn and Bacon The Hepatic-Portal System Carlson-Physiology of Behavior 6/e, Allyn and Bacon Glucoreceptors in Liver and Brain Carlson-Physiology of Behavior 6/e, Allyn and Bacon Eating Termination Signals relating to glucose and lipid start a meal What factors contribute to ending the meal? Head factors Sham-feeding studies suggest minimal impact of head factors on ending a meal Taste factors allow for learning about the caloric content of differing foods and can adjust subsequent intake Gastric factors The stomach is not required for feelings of hunger Nutrient receptors monitor calories in stomach Deutsch studies document that rats adjust their subsequent meals when food is withdrawn from their stomach via a fistula 13.* Carlson-Physiology of Behavior 6/e, Allyn and Bacon Eating Termination Intestinal factors Axons from the gut are sensitive to glucose, amino acids and fatty acids Food infusion into the duodenum suppresses sham-feeding in the rat CCK: a putative satiety hormone Released by entry of food into the duodenum Controls rate of stomach emptying Acts peripherally to reduce eating: vagotomy prevents the action of CCK on reducing eating CCK antagonists increase feeding Peptide YY3-36 (PYY): A peptide released by the gastrointestinal system after a meal in amounts proportional to the size of the meal. 13.* Carlson-Physiology of Behavior 6/e, Allyn and Bacon Eating Termination Glucoreceptors in the liver play a role in starting and stopping a meal Injections of glucose into peritoneal cavity reduced eating in hungry dogs, while similar IV injections did not Russek subsequently demonstrated that infusion of glucose into the hepatic portal vein produced long-lasting satiety in a hungry animal The hepatic portal vein is a direct route to the liver Infusion of small amounts of fructose into the hepatic portal vein also suppress eating; fructose does not cross into brain 13.* Carlson-Physiology of Behavior 6/e, Allyn and Bacon Long-term Satiety Body weight is a determinant of food intake Force-feeding studies: food intake falls as body weight increases Starvation studies: gastric satiety factors are less effective when body weight has been reduced below normal levels The fat cells of the body may produce a signal that represents amount of fat and that subsequently alters eating Leptin is a protein produced by fat that suppresses food intake and stimulates metabolism The genetically obese mouse (ob) lacks the gene that produces leptin Daily administration of leptin normalized weight in ob mice 13.* Carlson-Physiology of Behavior 6/e, Allyn and Bacon Neural Organization of Eating Brain stem circuitry can control feeding in the absence of the forebrain Decerebration involves a transection between the diencephalon and the midbrain Decerebrate rats can lick, chew, and swallow Motor neurons for eating are located in the brain stem AP/NST receives taste signals from tongue and hunger signals from the liver Lesions of the AP/NST abolish both glucoprivic and lipoprivic eating 13.* Carlson-Physiology of Behavior 6/e, Allyn and Bacon The Decerebrate Preparation Carlson-Physiology of Behavior 6/e, Allyn and Bacon Hypothalamic Regions Involved in Control of Eating Lateral hypothalamus Lesions of the LH produced undereating, electrical stimulation produced eating Is LH a ?feeding center?? Ventromedial hypothalamus Lesions of the VMH produced overeating, electrical stimulation suppressed eating Is VMH a ?satiety center?? 13.* Carlson-Physiology of Behavior 6/e, Allyn and Bacon LH Control of Eating Recent studies indicate a role for LH neurons in the control of eating Selective lesions of LH cell bodies reduce eating Excitation of LH cells by glutamate stimulates eating Glutamate antagonists in the LH reduce eating LH cells contain two peptide neurotransmitters Melanin-concentrating hormone (MCH) Orexin MCH and orexin infusions into the ventricles induce eating MCH/orexin neurons project to brain areas that modulate metabolism 13.* Carlson-Physiology of Behavior 6/e, Allyn and Bacon MCH and Orexin 13.* Carlson-Physiology of Behavior 6/e, Allyn and Bacon NPY Influences on Feeding The arcuate nucleus contains neurons that secrete neuropeptide Y (NPY) NPY acts to stimulate eating and to reduce metabolism (energy conservation) NPY neurons project to Paraventricular nucleus of hypothalamus (PVN) ? modulate metabolism Lateral nucleus of hypothalamus: induce eating (via action on MCH/orexin neurons) Food deprivation increases NPY levels in hypothalamus 13.* Carlson-Physiology of Behavior 6/e, Allyn and Bacon Brain Control Mechanisms Arcuate nucleus: A nucleus in the base of the hypothalamus that controls secretions of the anterior pituitary gland; contains NPY-secreting neurons involved in feeding and control of metabolism. Melanocortin-4 receptor (MC-4R): A receptor found in the brain that binds with ?-MSH and agouti-related protein; plays a role in the control of appetite. Agouti mouse: A strain of mice whose yellow fur and obesity are caused by a mutation that causes the production of a peptide that blocks MC4 receptors in the brain. Agouti-related protein (AGRP): A neuropeptide that acts as an antagonist at MC-4 receptors and increases eating Carlson-Physiology of Behavior 6/e, Allyn and Bacon Brain Control Mechanisms: Role in Satiety Ghrelin: A peptide hormone released by the stomach that increases eating; also produced by neurons in the brain. CART: Cocaine- and ampethamine-regulated transcript; a peptide neurotransmitter found in a system of neurons of the arcuate nucleus that inhibits feeding. ?-Melanocyte-stimulating hormone (?-MSH): A neuropeptide that acts as an agonist at MC-4 receptors and inhibits eating. Carlson-Physiology of Behavior 6/e, Allyn and Bacon Neuropeptide Y Interactions Carlson-Physiology of Behavior 6/e, Allyn and Bacon Neuropeptide Y Interactions Carlson-Physiology of Behavior 6/e, Allyn and Bacon Issues for Rational Therapies for Obesity Food intake and metabolism are controlled on multiple levels Intervention on one level may result in compensation on another level e.g. Subjects who overeat and stretch their stomach after stapling procedure Obesity is a multi-factorial disorder One therapy may not fit all Obesity is a long-term disorder: requires long-term treatments 13.* Carlson-Physiology of Behavior 6/e, Allyn and Bacon Obesity Obesity involves the excessive accumulation of fat Incidence of obesity is increasing Obesity is hazardous to health (diabetes, hypertension) Obesity is a disorder of metabolism (as well as eating) Body weight differences have a genetic component People vary in their metabolic efficiency (ability to convert and use consumed energy) Metabolic efficiency may reflect differences in Nonexercise activity thermogenesis (NEAT) Uncoupling protein (UCP2; a mitochondrial protein) in fat cells ? wastes energy by facilitating the conversion of nutrients into heat. 13.* Carlson-Physiology of Behavior 6/e, Allyn and Bacon Obesity Treatments Gastric stapling reduces stomach volume Intestinal bypass reduces food absorption Diarrhea and flatulence are problematic Bacterial overgrowth and vitamin deficiencies can occur after intestinal bypass surgery Pharmacological: Suppression of appetite (fenfluramine) Cardiac problems with fenfluramine (PPH, heart valve disorder) Herbal preparations that reduce appetite (ephedrine) Blockade of fat absorption (Xenical) Exercise can be of benefit in the treatment of obesity 13.* Carlson-Physiology of Behavior 6/e, Allyn and Bacon
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