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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