Control of Food Intake and Obesity Flashcards
outputs of energy
- mechanical work
- synthetic reactions
- membrane transport
- signal generation and conduction
- heat production
- degradation/detox
what organ is central to energy balance?
liver
4 fxns of liver in terms of energy balance
- conversion of nutrients to fuel for immediate use -> ATP and acetyl-coA
- short term use: glucose -> glycogen
- long term use: glucose, aa’s, fa’s -> TGs
- storage of fuels (glycogen, some TGs) `
3 phases of energy metabolism
- cephalic phase - preparatory
- absorptive phase
- fasting phase
what initiates the cephalic phase
sight, smell, expectation of food
describe insulin/glucagon levels during cephalic vs. absorptive vs. fasting phases
cephalic: insulin high, glucagon low
absorptive: insulin high, glucagon low
fasting: insulin low, glucagon high
what does insulin promote?
- glycogenesis in liver, muscle
- fat synthesis when glycogen stores full
what does insulin promote?
- glycogenesis in liver, muscle
- fat synthesis when glycogen stores full
during fasting, when the liver reserve of glycogen is used up, how is the supply of glucose for the brain ensured?
gluconeogenesis
what two areas of the brain control feeding behavior - what are their functions?
- lateral hypothalamus -> produces hunger
- ventromedial hypothalamus -> stops feeding
what does a bilateral lesion of the lateral hypothalamus cause?
aphagia (total loss of eating)
what does a lesion of the ventromedial hypothalamus cause? (3 effects)
- low satiation, excessive eating, weight gain, obesity
- overly responsive/aggressive (emotional disinhibition)
- abnormally high serum insulin (lose neural inhibition of secretion) and increased insulin secretion post-meal
describe neural mechanisms that control meal size, eating rate, and satiety
sensory signals from GI (stomach/intestinal filling, contents) -> vagus -> hormones in blood -> brainstem, hypothalamus
neurotransmitters and hormones that decrease feeding (9)
- serotonin
- norepi
- alpha-MSH
- CRH
- leptin
- insulin
- CCK
- enterostatin
- GLP-1
neurotransmitters and hormones that decrease feeding (9)
- serotonin
- norepi
- alpha-MSH
- CRH
- leptin
- insulin
- CCK
- enterostatin
- GLP-1
neurotransmitters and hormones that increase feeding (9)
- neuropeptide Y
- melanin-concentrating hormone
- orexins
- endorphins
- galanin
- aa’s (Glu, GABA)
- cortisol
- EXCESS insulin
- ghrelin
how does leptin work?
released by fat during lipogenesis -> decreases neuropeptide Y and CRH -> increases SNS activity -> increase metabolic rate -> increase energy expenditure, decrease insulin -> decreased energy storage, increase fat use (suppresses appetite)
where is ghrelin made?
endocrine cells in oxyntic gland area of stomach and some duodenum
difference between T1DM and T2DM
T1DM: destruction of beta cells -> don’t make insulin
T2DM: insulin resistance -> don’t respond to insulin
treatments for obesity (6)
- caloric restriction/dilution
- amphetamines
- sympathomimetic drugs (sibutramine)
- lipase inhibitors (orlistat)
- exercise
- bariatric surgery
mechanism of action for amphetamines
directly inhibit lateral hypothalamus -> suppress appetite and decrease food intake
mechanism of action for sympathomimetic drugs (sibutramine)
decrease food intake and increase energy expenditure -> decrease weight
mechanism of action for lipase inhibitors (orlistat)
reduce intestinal digestion of fat -> decrease energy intake -> decrease weight
what is a possible side effect of bariatric surgery?
malabsorption issues
