copyright16920xxbyallynandbacon

copyright16920xxbyallynandbacon内容摘要：

We Eat • Satiety – stops a meal, “being full” • Satiety signals – food in gut and glucose in the blood can induce satiety signals • Sham eating – satiety signals are not necessary for meal termination – Demonstrates the role experience plays in meal termination Factors That Influence How Much We Eat • Appetizer effect – small amounts of food may increase hunger – Due to cephalicphase responses? • Social influences – Even rats eat more when in a group • Sensoryspecific satiety – Eat more with a cafeteria diet – satiety is largely tastespecific Sensoryspecific Satiety • Tasting a food immediately decreases the positiveincentive value of similar tastes and decreases the palatability of all foods ~ 30 min later • Adaptive – encourages a varied diet Physiological Research on Hunger and Satiety • Role of blood glucose levels • Myth of hypothalamic centers • Role of the GI tract • Hunger and satiety peptides • Serotonin and satiety Role of Blood Glucose Levels in Hunger and Satiety • Blood glucose drops prior to a meal as preparation to eat – not a cue to eat • Must decrease blood glucose by 50% to trigger feeding • Premeal glucose infusions often do not suppress eating • Reduced blood glucose may contribute to hunger, but changes in blood glucose do not prevent hunger or satiety Myth of Hypothalamic Hunger and Satiety Centers • Experiments suggested 2 hypothalamic centers – Ventromedial (VMH) – a satiety center – Lateral (LH) – a hunger center • Lesion VMH hyperphagia • Lesion LH aphagia and adipsia Effect of bilateral VMH lesions Myth of Hypothalamic Hunger and Satiety Centers • VMH lesion rats maintain a new higher weight • LH lesion rats will recover if kept alive by tube feedin。