lec08.docx

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Department
Neuroscience
Course
NROC61H3
Professor
Rutsuko Ito
Semester
Fall

Description
lec08 long term food intake regulation 1. fat mass set point a. what happens if you go over or under the set point i. over 1. leptin / insulin levels increase 2. CART / POMC activated a. increase in a-MSH release 3. NPY / AgRP inhibited a. decrease in NPY / AgRP release 4. result: a. increased metabolism b. decrease in food intake ii. under 1. leptin / insulin levels decrease 2. NPY / AgRP activated a. increase in NPY / AgRP release 3. CART / POMC inhibited a. decrease in a-MSH release 4. result: a. decreased metabolism b. increased food intake regulatory mechanisms for feeding 1. food regulation a. long term effects b. short term effects i. episodic regulation regulation of meal size 2. short term maintenance of homeostasis 3. mediated by many factors a. internal b. external 4. meal termination is biologically controlled process 5. satiety signals can be overwritten model of short term regulation 1. 3 phases a. cephalic i. food cues elicit anticipatory activation of autonomic system b. gastric i. corresponds to time in which food consumption starts c. substrate i. when absorption is taking place meal initiation 2. external factors a. emotional factors i. sadness / breakup b. time of day i. conditioned to eat at certain times of the day c. availability and palatability of food i. foods that you like ii. usually has high calorie content d. threats from the environment i. stressors 3. internal factors a. orexigenic signal i. ghrelin 1. hunger signal  increases appetite 2. involved in both short and long term regulation of food intake meal termination 1. neurohormonal mediated event 2. hypothalamus may not be the center / key player in short term satiety signals short term satiety signals 1. gastric distension a. 2. cholecystokinin (CCK) a. stimulated in response to fat and protein injection in the gut b. released from duodenal cells c. local signals released directly into the gut in response to fat consumption d. transmitted by... i. vagus nerve ii. to nucleus tractus solitarius iii. to brain stem (hindbrain) iv. to hypothalamic region (forebrain) 3. meal termination is mediated by structures in the hindbrain, not the forebrain a. animals without a hypothalamic region i. will be able to meal terminate ii. will not be able to regulate the long term homeostatic set point iii. will not be able to meal initiate CCK 1. mediates pre-absorptive satiating effect of fats a. anticipatory aspect b. may be critical in regulating the intake of fat 2. a receptor binding is important 3. direct association between CCK and fat consumption CCK-a knockout model 1. average meal size increases in knockout rats 2. consume more food in comparison to wildtype 3. meal numbers actually decrease  but get fat because they consume much more per meal overriding satiety -- overeating 1. sensory specific satiety a. can eat a lot more eating at a buffet i. can get sated on one taste very quickly ii. a new taste can overcome satiety iii. more choices  more satiety 2. emotional / social factors a. eating in group vs eating alone 3. hedonics a. palatability homeostasis and hedonics 1. nutritional need state a. depletion  hedonic response enhanced (experienced palatability or pleasure) b. repletion  hedonic effect is reduced (satiation) 2. don't need food  still want it a. e.g. desert cafeteria diet model in rats 1. give a rat a choice between lab chow or palatable foods a. lab chow b. junk food i. rats prefer junk food ii. over consume  become obese 1. still consume these foods even if there are adverse consequences for these foods interaction between hedonia neural systems and homeostatic mechanisms 1. leptin signals become defective when hypothalamic endocannabinoid levels are high a. endocannabinoid levels involved in hedonic system i. liking / palability 2. consuming highly palatable foods  neural circuitry involved are a little different a. involves taste processing  reward circuit  effect on satiety highly palatable foods 1. drive to eat is not necessarily maintained by biological needs of animal a. but is maintained by reward circuit for sure 2. increases NPY / AgRP  increased food intake 3. ...slide 16 outside of the hypothalamus 1. downstream  brainstem a. fundamental aspects of consumption not affected by decerebration b. ...slide 17 2. upstream  limbic system a. choosing foods activated orbitofrontal cortex (connected to the medulla) b. EXAM: i. support or not support a statement  need evidence (should know author's name) c. ...slide 18 drinking and thirst 1. why do we drink? basic facts 2. human body cannot create fluid 3. lot of water content in body a. 67% is intracellular i. fluid portion of cytoplasm b. 33% is extracellular i. e.g. CSF 4. need to maintain a certain osmotic pressure 5. fluctuation in plasma osmotic pressures a. react very quickly to changes in osmotic pressures b. very sensitive c. note: referring to OSMOLARITY osmosis - terminologies 1. isotonic a. no movement of fluid between two compartments 2. hypertonic a. water moves out of cell b. too much solute 3. hypotonic a. water moves into cell b. too little solute fluid regulation 1. normally the intersitial fluid is isotonic with intracellular fluid 2. total volume of body fluid must be regulated 3. if blood volume is too low  heart can no longer pump blood effectively 4. two sets of osmoreceptors a. intracellular fluid volume receptors b. blood volume receptors two types of thirst 1. osmotic thirst a. triggered by cellular dehydration i. induce this by adding salt into interstitial fluid
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