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Physio - GI > Control of Food Intake and Obesity > Flashcards

Control of Food Intake and Obesity Flashcards

1
Q

outputs of energy

A
  • mechanical work
  • synthetic reactions
  • membrane transport
  • signal generation and conduction
  • heat production
  • degradation/detox
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2
Q

what organ is central to energy balance?

A

liver

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3
Q

4 fxns of liver in terms of energy balance

A
  1. conversion of nutrients to fuel for immediate use -> ATP and acetyl-coA
  2. short term use: glucose -> glycogen
  3. long term use: glucose, aa’s, fa’s -> TGs
  4. storage of fuels (glycogen, some TGs) `
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4
Q

3 phases of energy metabolism

A
  1. cephalic phase - preparatory
  2. absorptive phase
  3. fasting phase
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5
Q

what initiates the cephalic phase

A

sight, smell, expectation of food

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6
Q

describe insulin/glucagon levels during cephalic vs. absorptive vs. fasting phases

A

cephalic: insulin high, glucagon low
absorptive: insulin high, glucagon low
fasting: insulin low, glucagon high

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7
Q

what does insulin promote?

A
  • glycogenesis in liver, muscle

- fat synthesis when glycogen stores full

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8
Q

what does insulin promote?

A
  • glycogenesis in liver, muscle

- fat synthesis when glycogen stores full

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9
Q

during fasting, when the liver reserve of glycogen is used up, how is the supply of glucose for the brain ensured?

A

gluconeogenesis

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10
Q

what two areas of the brain control feeding behavior - what are their functions?

A
  • lateral hypothalamus -> produces hunger

- ventromedial hypothalamus -> stops feeding

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11
Q

what does a bilateral lesion of the lateral hypothalamus cause?

A

aphagia (total loss of eating)

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12
Q

what does a lesion of the ventromedial hypothalamus cause? (3 effects)

A
  • 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
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13
Q

describe neural mechanisms that control meal size, eating rate, and satiety

A

sensory signals from GI (stomach/intestinal filling, contents) -> vagus -> hormones in blood -> brainstem, hypothalamus

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14
Q

neurotransmitters and hormones that decrease feeding (9)

A
  • serotonin
  • norepi
  • alpha-MSH
  • CRH
  • leptin
  • insulin
  • CCK
  • enterostatin
  • GLP-1
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15
Q

neurotransmitters and hormones that decrease feeding (9)

A
  • serotonin
  • norepi
  • alpha-MSH
  • CRH
  • leptin
  • insulin
  • CCK
  • enterostatin
  • GLP-1
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16
Q

neurotransmitters and hormones that increase feeding (9)

A
  • neuropeptide Y
  • melanin-concentrating hormone
  • orexins
  • endorphins
  • galanin
  • aa’s (Glu, GABA)
  • cortisol
  • EXCESS insulin
  • ghrelin
17
Q

how does leptin work?

A

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)

18
Q

where is ghrelin made?

A

endocrine cells in oxyntic gland area of stomach and some duodenum

19
Q

difference between T1DM and T2DM

A

T1DM: destruction of beta cells -> don’t make insulin
T2DM: insulin resistance -> don’t respond to insulin

20
Q

treatments for obesity (6)

A
  • caloric restriction/dilution
  • amphetamines
  • sympathomimetic drugs (sibutramine)
  • lipase inhibitors (orlistat)
  • exercise
  • bariatric surgery
21
Q

mechanism of action for amphetamines

A

directly inhibit lateral hypothalamus -> suppress appetite and decrease food intake

22
Q

mechanism of action for sympathomimetic drugs (sibutramine)

A

decrease food intake and increase energy expenditure -> decrease weight

23
Q

mechanism of action for lipase inhibitors (orlistat)

A

reduce intestinal digestion of fat -> decrease energy intake -> decrease weight

24
Q

what is a possible side effect of bariatric surgery?

A

malabsorption issues

Physio - GI (5 decks)

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