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Homeostasis
Food and Energy
| Terms | Definition | . |
|---|---|---|
| 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
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