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Food and Energy

Food Utilization •Efficiency (25%) •Processing of new food (8%) •Basal metabolism (55%) •Active behavior (12-13%) Futility of Dieting: Basal metabolism decreases, but body weight does not
Carbohydrates •sugars, starches, celluloses, gums •Main source of energy = glucose (simple carbo) •Converted to and from glycogen (complex carbo) Pancreas Hormone Liver Beta cells -> Insulin -> glucose stored as glyocogen Alpha cells -> Glucagon -> glucose converted from glycogen
Glucose Pathway Liver glucodetectors signal Pancreas (via vagus and NST ) To increase insulin Glucose transporters + insulin -> glucose in cells Liver (via vagus) -> NST < -> HTNST -> pancreas
Stored Glucose •Main source of energy = glucose (simple carbo) •Converted to and from glycogen (complex carbo) •Carboscan be stored inlongtermform as fats -Can be used as ketonesor fatty acids later -Brain needs glucose (but not insulin)
Food Intake Phases •cephalic phase •digestive phase •absorptive phase
Diabetes Mellitus •Type I vs Type II •Possible causes •Health implications •Hunger
Satiety Signal Condidates •insulin -no •glucose -no •gut distension -small contribution maybe •gut peptides-yes but not the only signal
CCK: Cholecystokinin •Gut peptide-duodenum. •Released especially if high fat/protein foods eaten. •Also made and released by brain neurons. •Rat and human studies.
Neuropeptide •NPY fromarcuateto PVN-seems to stimulate feeding. •Orexins-from lateral hypothalamus, stimulate feeding. •leptinstimulates release of CRH,melanocortin, andneurotensin.
Old Theory: Dual Center •VMH initially felt to be a satiety center (lesions=weight gain) BUT: new higher set point is defended, and satiety occurrs ALSO: Lesions may have damaged fibers of passage from PVN. Rats appear more finicky-lose weight if food is made bitter. •LH initially thought to be a hunger center (lesions = weight loss) BUT: New lower set point is defended; and hunger occurs. ALSO: Drinking affected as well as feeding. •Similar effects are seen in humans with hypothalamic lesions.
LEPTIN MODEL 1. fat cells secrete leptin. (the larger the fat cells, the more leptin is secreted) 2. Leptin reaches leptin receptors in hypothalamic regions (LH, arcuate, supraoptic, paraventricular nuclei) 3. Leptin receptor activation suppresses neuropepetide production and release (which normally trigger hunger) 4. Receptor activation also increases levels of hunger suppressing CRH, and melanocortin
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Created by: brown55