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【文章內(nèi)容簡介】 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
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