Term
| Lateral hypothalamus - FEED ME |
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Definition
Stomach and small intestines secrete ghrelin which increases NPY stimulating *feeding center*
•Bilateral lesion will make you never want to eat and will starve
•Stimulation causes voracious eating (hyperphagia)
•Directly excites the emotional drive to search for food
•Excites brain stem centers controlling chewing, salivation, swallowing
•Inhibited by stimulation of satiety center |
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Term
| Ventromedial hypothalamus - I'M STUFFED |
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Definition
Fat stores cause release of leptin which decreases NPY stimulating the *satiety center*
• Lesion VMH and you will never feel full and will overeat
• Stimulation causes complete satiety; acts by inhibiting hunger/feeding center. |
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Term
| Neurotransmitters/hormones that affect hypothalamus |
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Definition
• Leptin decreases NPY decreasing feeding
• Insulin, CCK, NE, melanocyte stimulating hormone, CRH, CART, GLP-1 also decrease feeding
• Neuropeptide Y (NPY) increases feeding when increased
• Ghrelin, Melanin concentrating hormone, orexins A & B, endorphins, galanin, cortisol, amino acids also increase feeding
- Ghrelin: made in stomach and small intestines by parietal cells, stimulated by decreased energy stores, levels increase pre-prandial but is not a catalyst to hunger (is a meal initiation signal, starts to be secreted an hour or two before we eat). Gastric bypass reduces levels. Production peaks around 1-2am. It acts on the hypothalamus (arcuate nucleus) |
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Term
| Other neural centers that influence feeding |
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Definition
• Brain stem – mechanics of feeding, salivation, licking lips, chewing, swallowing
• Amygdala – some areas increase feeding while others decrease it; bilateral lesion will cause “psychic blindness” in choice and quality of food (they will eat anything no matter how rotten or gross it is)
• Prefrontal cortex (or cortical areas of the limbic system) – responsible for determining quality of food that is ingested (remembers previous unpleasant experience such as food poisoning)
• Hypothalamus – controls quantity of food intake |
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Term
| Short term regulation of satiety |
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Definition
• Feeding stops prior to nutrient absorption
• Oral receptors – the number of times we chew/swallow meters how much food we are eating. Inhibition lasts about 30 mins
• GI filing – distention of GI tract, stomach, and duodenum; stretch inhibitory signals transmitted mainly by way of vagi to suppress feeding center; inhibition lasts 1-2 hours
• GI hormones – CCK, glucagon and insulin all suppress feeding; CCK released mainly in response to fat entering duodenum; presence of food in stomach and duodenum causes the pancreas to secrete significant quantities of glucagon and insulin. Inhibition lasts around 2 hours |
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Term
| Intermediate term regulation of satiety |
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Definition
• Glucostatic theory – high blood glucose and/or high level of glucose metabolism stimulates satiety center
• Aminostatic theory – a decrease in blood amino acid precursor concentrations will cause hunger (W, Y, choline); very potent satiating nutrient
• Lipostatic theory – a decrease in blood lipid concentrations will cause hunger and vice versa. Least potent satiating nutrient despite the CCK release
• Temperature regulation – when cold an animal will overeat (increases metabolism, want fat insulation), when hot it will undereat
• Caused by interaction within the hypothalamus between temp-regulating system and food intake-regulating system
• Feedback signals from adipose tissues
• body fat stores is regulated variable and any deviation will change feeding behavior; hypothalamic receptors monitor levels of fat metabolites which signal size of body fat stores
• activated if short-term regulators fail and body weight deviates out of range; adipose mass is the most likely regulated factor; leptin signals the energy storage to the hypothalamus
• increase in adipose tissue -> ob gene in adipose tissue becomes active -> synthesis and release of leptin into bloodstream -> hypothalamus stimulated -> appetite decreased by decrease in NPY and increase in CRH -> hunger decreases, SNS increases -> decreased food intake, increased metabolism/energy expenditure, decrease insulin secretion and energy storage
• Leptin – produced by white adipose tissue (adipocytes), acts on hypothalamus, down-regulated by decreased fat mass, reduced food intake and lowers body weight by decreased NPY (appetite suppression) and insulin (decreased storage) and an increase in CRG (decreased food intake) and SNS activity (higher metabolic rate) |
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