Pinel - Hunger, Eating and Health

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Lecture 10a THE DUAL-CENTER SET-POINT MODEL OF EATINGCOURSE MATERIAL AND Pinel LECTURE NOTES Outline: 1. 2. 3. 4. 5. The Early Studies Glucostatic and Lipostatic Theories v. Positive-Incentive Theories a. Glucostatic and Lipostatic Theories b. Positive-Incentive Theories Hypothalamic Hunger and Satiety Centers and The Dual-Center Set-Point Model a. Ventromedial Hypothalamus b. Lateral Hypothalamus Positive-Incentive Models of Feeding Current Research on the Biopsychology of Eating a. Palatability and Positive Incentives b Energy Expenditure and Body-Fat Homeostasis c. Satiety Peptides d. Reevaluation of the Role of the Ventral Hypothalamus e. Role of Learning in Eating A Settling-Point Model of Body-Weight Regulation

6.

Lecture Notes 1. The Early Studies (use Digital Image Archive Figure CH10F01.BMP)

Energy is available to the body in three forms: (1) lipids (fats), (2) proteins (broken into amino acids), and (3) glucose (simple sugar byproducts of carbohydrates) Energy metabolism occurs in three phases (use Digital Image CH10F03.BMP); open in browser PRO version

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1) the cephalic phase (preparatory), 2) absorptive phase (energy absorbed into the bloodstream), and 3) the fasting phase (body utilizes food stores) The first influential study of the physiological basis of hunger was conducted in 1912 by Canon and Washburn; Washburn swallowed a balloon on the end of a thin tube, the balloon was partially

inflated, and a pressure gauge was attached to the other end of the tube each time that he had a large stomach contraction, Washburn reported a pang of hunger; this led to the view that stomach contractions are a major factor in hunger. But the finding that animals whose stomachs had been denervated or completely removed ate enough to maintain their body weights discredited this view; in addition, people with no stomachs report feeling hungry and maintain their body weights; they eat less per meal, but they eat more meals More recently, Koopman (use Digital Image Archive Figure CH10F12.BMP) has used a second-stomach preparation to implicate the gut in feeding behavior; Rats who have had a second stomach implanted into their peritoneum eat less when the second stomach is loaded with food, even though the stomach is not innervated nor are the nutrients able to be absorbed into the bloodstream. 2. Glucostatic and Lipostatic Theories of Hunger research on feeding has been heavily influenced by the idea of a feeding set-point, open in browser PRO version

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research on feeding has been heavily influenced by the idea of a feeding set-point, based around the idea of a homeostatic, negative feedback system regulating feeding. research on feeding has been strongly influenced by the idea that feeding is controlled by deviations from two different set points: 1. a set point for blood glucose (short-term regulation) and 2. a set point for body fat (long-term regulation) 3. Hypothalamic Hunger and Satiety Centers and The Dual-Center Set-Point Model

In the 1950's, studies in which various areas of the rat hypothalamus were lesioned or stimulated seemed to suggest that it contained the hypothesized hunger and satiety centers a. Ventromedial Hypothalamus (VMH) (use Digital Image CH10F08.BMP)

Large bilateral lesions of the VMH produced hyperphagia and gross obesity; after the lesion, the rats were extremely hyperphagic and gained weight rapidly (dynamic phase); after several weeks hyperphagia was only slight and a new very high body weight was defended (static phase) although several nuclei were damaged by the large VMH lesions, the syndrome was typically attributed to ventromedial nucleus damage two interpretations were proposed: (1) that glucoreceptors and their associated satiety circuits had been destroyed, or open in browser PRO version

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