Food and Energy
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| 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
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| 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
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| 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
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| 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) |
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| Food Intake Phases | •cephalic phase •digestive phase •absorptive phase |
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| Diabetes Mellitus | •Type I vs Type II •Possible causes •Health implications •Hunger |
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| Satiety Signal Condidates | •insulin -no •glucose -no •gut distension -small contribution maybe •gut peptides-yes but not the only signal |
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| CCK: Cholecystokinin | •Gut peptide-duodenum. •Released especially if high fat/protein foods eaten. •Also made and released by brain neurons. •Rat and human studies. |
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| Neuropeptide | •NPY fromarcuateto PVN-seems to stimulate feeding. •Orexins-from lateral hypothalamus, stimulate feeding. •leptinstimulates release of CRH,melanocortin, andneurotensin. |
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| 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.
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| 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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