19 | Appetite Flashcards

1
Q

satiety

A

feeling of fullness

  • peptides
  • gastric distention
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2
Q

satiety peptides

A

appetite-inhibitory peptides (released from GI)
-CCK (cholecystokinin)
-GLP-1 (glucagon like peptide, also incretin - improves glucose tolerance during a meal)
decrease appetite by delaying rate of gastric emptying, slowing return of hunger
major short-term endocrine regulators of appetite

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3
Q

satiety signals (3)

A
  • vagal pathways
  • short acting
  • define meal size and frequency
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4
Q

ghrelin (4)

A

only gut peptide that increases appetite

  • binds to appetite stimulator neurons in hypothalamus
  • increases food intake and body weight
  • decreases fat breakdown (dec. energy use)
  • level inc before meal (hunger), fall after a meal (fed)
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5
Q

insulin (3)

A

-responds to levels of nutrients, affects their metabolism/energy use
-crosses BBB, binds to hypothalamus neurons that suppress appetite
(dec meal size and freq is a way for insulin to dec BG)
-adiposity hormones, levels parallel amount of adipose

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6
Q

adipose tissue

A

metabolic endocrine “organ”

  • brown fat: rich in mitochondria, thermogenesis
  • white fat: energy storage, breakdown releases FFA’s and glycerol. endocrine center. receptors for response to metabolic and endocrine signals. secretes hormones and cytokines. metabolism of steroid hormones.
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7
Q

leptin

A
  • secreted by adipose tissue
  • binds to hypothalamus neurons, inhibits appetite
  • many obese people are leptin (+ insulin) resistant, rather than deficient
  • adiposity signal, levels correlate with adipose
  • rapid drop during fasting, can influence other hormonal axes (loss of menstrual periods with strenuous exercise or malnutrition)
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8
Q

longer term appetite regulators

A

leptin + insulin: inhibit appeptite

ghrelin: opposes action of leptin
- peripheral effectors

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9
Q

exercise + energy homeostasis

A

-promotes negative energy balance (energy use > food intake, weight loss)
-improvees insulin sensitivity and glucose uptake in skeletal muscle, overcome insulin resistance
acute exercise:
-promotes post prandial levels of satiety peptides
-ghrelin levels may decrease
-leptin levels fall long term

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10
Q

orexigenic circuit

A

appetite stimulating

  • food intake, energy conservation signals
  • activated by ghrelin
  • inhibited by leptin
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11
Q

anorexigenic circuit

A

appetite inhibiting

-activated by leptin

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12
Q

hypothalamus

A

ARC region: anorexigenic and orexigenic nuerons
-receptors for ghrelin + leptin
-activation releases neuropeptides
-activate second order neurons associated with weight loss or gain pathways
-net signals to higher cortical centers and limbic system
(circuits active at same time, varying levels to fine tune appetite and energy use. prolonged imbalance - net weight gain or loss)

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13
Q

hungry state

A
  • inc ghrelin activates orexigenic receptors
  • secrete neuropeptide Y (NPY) and agouti-related peptide (AgRP)
  • activate second order neurons with NPY-R
  • initiates feeding behaviors, metabolic processes
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14
Q

fed state

A
  • leptin activates anorexigenic receptors (and inhibit orexigenic)
  • neurons release CART (cocaine + amphetamine related transcript) and POMC (pro-opiomelanocortin) peptides
  • POMC cleaved to a-MSH, binds to melanocortin-rec on second order neurons
  • inhibit feeding behavior, promote energy use
  • path can be overriden by AgRp
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15
Q

melanocortin receptor + obesity

A

-receptor defects
-chronic inhibition by AgRp
can cause obesity, interruption of anorexigenic signals

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16
Q

visual cues

A
  • tend to eat more with larger package, utensils, food portions
  • cue of how much eaten can signal to stop eating
17
Q

energy density

A
  • amount of energy/g of food (kcal/g)
  • modulates overall energy intake
  • low energy dense meal with comparable levels of fullness can decrease intake
18
Q

sensory perception

A

food taste, smell, appearance

-can influence palatability, and amount eaten

19
Q

Pima Indian study + thrifty gene hypothesis

A

Pima Indians - genetically predisposed to obesity + T2DM

  • two genetically identical populations, one in S. Arizona, other in remote Mexico
  • US group had more sedentary lifestyle, easier access to high cal, processed foods
  • Mexican group had higher activity levels, consume lower-fat, traditional foods
  • in Mexican group, obesity was uncommon and prevalence of T2DM was comparable to US population (8% overall)
  • but in US group almost half had T2DM, and 95% of them were obese

support thrifty gene hypothesis:
ability to accumulate and retain stores of fat is adaptational in time of famine
-shows primary influence of environmental factors on genetic predisposition to obesity and T2DM

20
Q

metabolic syndrome

A

conditions that increase risk of coronary artery disease
-obesity
-hypertension
-T2DM
-cholesterol abnormalities
[high insulin levels, with inc fasting glucose or glucose intolerance and central obesity, abnormal cholesterol, or high BP]