Chapter 12 Hunger, Eating, and HealthControl of EatingDigestion and Energy FlowEnergyEnergy MetabolismSlide 6Set point systemsWhat’s the set-point?Problems with Set-Point TheoriesSlide 10Positive-Incentive PerspectiveFactors That Determine What We EatWHEN We EatHow Much We EatSlide 15Physiological Research Hunger and SatietyRole of Blood Glucose LevelsMyth of Hypothalamic Hunger and Satiety CentersMyth of Hypothalamic Hunger and Satiety CentersSlide 20Role of the Gastrointestinal Tract in SatietySlide 22Satiety PeptidesHunger PeptidesSerotonin and SatietySlide 26Slide 27More Problems…Slide 29Why do we care?Why Is There an Epidemic of Obesity?Mutant Obese Mice and LeptinInsulin: Another Negative Feedback SignalChapter 12Hunger, Eating, and Health1Control of Eating•Is there a “set point” for the body’s energy reserves that determines when we eat?2Digestion and Energy Flow•Digestion – breaking down food and absorbing its constituents•3 forms of energy –Lipids (fats)–Amino acids (proteins)–Glucose (carbohydrates)3Energy •Delivered to the body as lipids, amino acids, and glucose•Stored as fats, glycogen, and proteins–Most stored as fats.4Energy Metabolism•Cephalic phase – preparation•Absorptive phase – energy absorbed•Fasting phase – energy from reserves56Set point systems•Negative feedback systems•Homeostasis: a constant internal environment7What’s the set-point?•Glucostatic theories – glucose levels–Meal initiation and termination•Lipostatic theories – fat stores–Long-term regulation8Problems with Set-Point Theories•Epidemic of eating disorders•Contrary to evolutionary pressures that favored energy storage for survival9Problems with Set-Point Theories•Reductions in blood glucose or body fat do not reliably induce eating•Do not account for the influence of external factors on eating and hunger 10Positive-Incentive Perspective•We are drawn to eat by the anticipated pleasure of eating – we have evolved to crave food•Accounts for the impact of external factors on eating behavior11Factors That Determine What We Eat•Adaptive species-typical preferences–Sweet and fatty foods – high energy–Salty – sodium-rich•Adaptive species-typical aversions–Bitter – often associated with toxins12WHEN We Eat•Approaching mealtime…–Cephalic phase leading to a decrease in blood glucose•Pavlovian conditioning of hunger13How Much We Eat•Satiety – stops a meal, “being full”•Sham eating–Demonstrates the role experience plays in meal termination14How Much We Eat•Appetizer effect–Small amounts of food may increase hunger •Social influences–Even rats eat more when in a group•Sensory-specific satiety–Eat more with a cafeteria diet – satiety is largely taste-specific15Physiological Research Hunger and Satiety•Role of blood glucose levels•Myth of hypothalamic centers•Role of the GI tract•Hunger and satiety peptides•Serotonin and satiety16Role of Blood Glucose Levels•Blood glucose drops prior to a meal as preparation to eat – not a cue to eat•Reduced blood glucose may contribute to hunger, but changes in blood glucose do not prevent hunger or satiety17Myth of Hypothalamic Hunger and Satiety Centers•Two hypothalamic centers–Ventromedial (VMH) – a satiety center–Lateral (LH) – a hunger center•Lesion VMH > hyperphagia •Lesion LH > aphagia and adipsia18Myth of Hypothalamic Hunger and Satiety Centers•Hypothalamus – regulates energy metabolism19Myth of Hypothalamic Hunger and Satiety Centers•VMH lesions increase blood insulin–Lipogenesis (fat production) increases–Lipolysis (fat breakdown) decreases–All calories are quickly stored so the rat must eat more to meet immediate needs20Role of the Gastrointestinal Tract in Satiety•Cannon and Washburn (1912)–Studies suggested stomach contractions led to hunger, distension to satiety•Blood-borne satiety signals?2122Satiety Peptides•Gut peptides that decrease meal size:–Cholecystokinin (CCK), bombesin, glucagon, somatostatin•Must 1st establish that peptide does not merely create illness23Hunger Peptides•Usually synthesized in the hypothalamus - neuropeptide Y, galanin, orexinA, ghrelin•Many different signals control eating•Hypothalamus plays a central role 24Serotonin and Satiety•Serotonin agonists consistently reduce rats’ food intake–Even intake of palatable food is affected –Reduces amount eaten per meal–Preferences shift away from fatty foods•Similar effects seen in humans25Problems with Set-Point Theories•Variability of body weight•Set points and health–Free-feeding does not lead to optimum health–Positive effects seen with caloric-restriction2627More Problems…•Altering metabolism•Diet-induced thermogenesis – increases in body fat increase body temperature2829Why do we care?•Can control our body weight•Then why is there an obesity epidemic?30Why Is There an Epidemic of Obesity?•Evolution favored preferring high calorie food, eating to capacity, storing fat, & using energy efficiently•Cultural practices and beliefs promote consumption31Mutant Obese Mice and Leptin•Mice are 3X normal weight–Lack leptin, a hormone produced by fat cells•Leptin – a negative feedback fat signal32Insulin: Another Negative Feedback Signal•Like leptin, –levels correlated with body fat–receptors found in the brain–reduces eating at levels too low to be aversive or to affect blood glucose•Insulin deficiency leads to hyperphagia, but not obesity – food not converted to fat in the absence of