Appetite Regulation and Obesity Flashcards

1
Q

Homeostatic controls

A
  • like a feedback regulated thermometer
  • include:
    hypothalamus, brainstem, and nucleus solitary track
  • hormones (leptin, CCK, GLP-1) work through this regulated system
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2
Q

Hedonic Feeding

A
  • not really regulated and responds to reward or other environmental stimuli
  • includes:
    parts of the brain like the cortex and nucleus accumbens
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3
Q

AgRP/NPY neurons

A
  • inhibited by leptin and insulin
  • increase appetite (ghrelin increases NPY to increase appetite)
  • decrease energy expenditure
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4
Q

POMC/CART neurons

A
  • have opposite effect of AgRP/NPY
  • decrease ghrelin
  • stimulated by leptin and insulin

DECREASE appetite
INCREAE energy expenditure

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5
Q

Satiety

A

the feeling of fullness that persists after eating and suppress further consumption

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6
Q

Satiation

A

the process that causes one to stop eating

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7
Q

Ghrelin (function)

A

high at start of a meal, but rapidly declines after food intake

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8
Q

Leptin (function)

A
  • influences appetite center in hypothalamus
  • low leptin levels decreases sensitivity to satiation signals
  • high leptin levels means you’ll feel full when you’re supposed to
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9
Q

CCK (function)

A
  • responsive to fat and protein intake

- rapidly reduces meal size and duration

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10
Q

PYY (function)

A
  • responsive to fat intake

- decreases food intake by 30%

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11
Q

High ghrelin levels

A

Grhelin levels increase as a way for you to eat and gain weight

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12
Q

Low ghrelin levels

A
  • typically low in obese people because they are trying to drive down intake and regulate body weight
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13
Q

Leptin Discovery

A
  • discovered leptin was the hormone missing from ob/ob mice, and the db/db mouse had enough leptin, but was resistant to it
  • humans who are obese are leptin deficient
  • leptin will not cure obesity unless that person can’t produce leptin
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14
Q

Adipokine

A
  • any hormone that is released in response to how much fat tissue you have and is released from fat cells
  • Examples: leptin, insulin, and adiponectin
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15
Q

How is obesity defined?

A

BMI cut-offs

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16
Q

Evidence obesity is caused partly by genetics

A

Twin studies where twins have similar body sizes

- BMI and fat distribution were similar

17
Q

Genes associated with obesity

A
  • Leptin, Leptin receptor, MC4R, POMC

- FTO related to common obesity

18
Q

Environmental changes that contribute to increases in obesity

A

smoking, diet, physical activity, toxins, intrauterine conditions, and stress

19
Q

Why is obesity associated with so many metabolic diseases?

A
  • it promotes an inflammatory response
  • when cells get too big they release cytokines (Ex: tnf-alpha)
  • results in insulin resistance (starts in muscles and then fat cells)