Pomc neurons release αmsh cart are activated by

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POMC neurons (release αMSH & CART) are activated by leptin and insulin. X - + NPY/AgRP and POMC neurons have reciprocal inhibition.
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dorsal hindbrain
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Internal Signals that Regulate Feeding Behavior Research has revealed: Effects of peptides (hormones and neurotransmitters) on feeding Redundant systems Direct or indirect Effects? Energy balance, feeding, thermoregulation and metabolic rate Food provides nutrients and energy for cellular function, as well as, energy for thermoregulation (uses most of energy). Feeding behavior needs to be prospective to prevent shortages. Brain monitors energy stores to anticipate needs; stores ensure that energy will be available.
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Presuming feeding reflects internal states of hunger and satiety, it is postulated that meal consumption (i.e. food) triggers satiety signals that inhibit further feeding via a negative feedback loop. Satiety Signals and the Short-Term Control of Feeding
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Satiety Signals Head factors Mouth and mouth movements, chewing, etc. Send information via 3 cranial nerves to the nucleus of the solitary tract (NST) Gastric factors Stretch receptors in the stomach Also can detect nutrients Send information via the vagus nerve to the NST
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Gastric Satiety Signals Gastric distention Stomach endowed with stretch receptors Vagus to NST & area postrema Cholecystokinin Secreted during meals Receptors on Vagal afferent fibers that also convey gastric stretch signals CCK + stretch act synergistically to inhibit food intake Bombesin: found throughout GI tract and nervous system Injection decreases food intake Effects of Bombesin and CCK additive Mechanism of action: unknown but not vagal Extent of role in normal feeding unknown Post-gastric Nutritional signals from intestines to liver or pancreas e.g. glucose.
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Satiety Signals Intestinal factors Contains nutrient receptors Glucose, amino acids, & fats Duodenum contains liporeceptors Fat in the duodenum causes the release of cholecystokinin (CCK) CCK causes the gall bladder releases bile CCK is possibly a satiety factor Receptors in the hypothalamus
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Satiety Signals Liver factors First organ to learn that food has been received from intestines Glucoreceptors Experiment with fructose vs. glucose injection to the hepatic portal vein Both injections caused rats to eat less Suggests that the liver sends a satiety signal to the brain
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Long Term Satiety Signal Leptin Peptide released by adipose tissue Receptors in the hypothalamus (arcuate nucleus) Genetically engineered mice with two different genetic mutations either: ob/ob mice db/db mice 2 kinds of problems Lack of the ability to make leptin Leptin insensitivity
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Leptin switches from carb (glucose) to fat usage (lipolysis). Aided by catecholamines (CAT) via Sympathetic NS and T3 Leptin acts via a Gs receptor which via AC/cAMP/PKA prodution phosphorylates hormone sensitive lipase to start lipolysis (I.e burn fat)
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