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U6 MCP > Obesity 1 - CB > Flashcards

Obesity 1 - CB Flashcards

1
Q

What BMI is considered underweight?

A

<18.5

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2
Q

What BMI is considered normal?

A

18.5-24.9

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3
Q

What BMI is considered overweight?

A

25-29.9

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4
Q

What BMI is considered grade 1 obese?

A

30-34.9

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5
Q

What BMI is considered grade 2 obese?

A

35-39.9

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6
Q

What BMI is considered grade 3 obese?

A

> 40

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7
Q

Why is BMI imperfect?

A

doesnt account for sex or racial differences, fat to muscle ratio, or visceral vs subcutaneous fat

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8
Q

how do you measure regional adioposity?

A

waist to hip ratio (normal females <1.0) and waste to height ratio

skin fold thickness

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9
Q

Risks of being fat:

A

developing type 2 DM
cardiovascular disease
joint disease, gallbladder disease, reproductive disorders, obstructive sleep apnea, some cancers (hematological, pancreatic, prostate, postmenopausal breast)

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10
Q

Fact: Americans are fat,
50% of us are overweight or more BMI >25
35% of adults and 17% of children are obese BMI >30
5% are extreme obese >40

A

This costs the US so much money in health care (But it makes us money yay fat people!!!!)

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11
Q

Causes of obesity:

A

Genetics: polygenic mostly
environment: bad diet, lack of excercise
Gut Microflora
number of adipocytes established early in life

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12
Q

Fact: It appears the biological system seems to be resistant to long term weight changes.

A

so “the biggest looser” show is a hoax

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13
Q

What is lipostat? what must a lipostat have?

A

A postulated idea that a persons body weight is regulated around a set point? (like a thermostat)

Needs a signal, a sensor, and effectors that mediate food intake and energy expenditure

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14
Q

What is the fat to brain signaling system? What are the parts to it (signal, sensor, effectors)?

A

A lipostat like system

sensor: leptin (hormone like protein)
receptor: leptin receptor (in hypothalamus)
Effectors: orexigenic: promotes feeding (hypothalamic)
anorexigenic: supressed feeding (hypothalamic)
energy expenditure factors

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15
Q

True or False: the circulating leptin levels are proportional to the fat accumulation.

A

True

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16
Q

What mediates leptin levels? what does increased leptin cause? decreased? Stable?

A

body fat levels, increase in fat increases leptin levels causing the body to eat less and spend more energy. Decrease in at causes a decrease in leptin and you eat more, stable weight= stable leptin= food in = food out

17
Q

What happens to leptin in longterm weight gain?

A

The “set point” level of leptin is increased causing obesity, but food intake will eventually equal the energy expenditure at the new obese weight

18
Q

What happens to the sensitivity of leptin in obese people?

A

it decreases, the lipostat system “defends” the obese state. in general lipostat tries to maintain a constant weight

19
Q

How do mice with a homozyous deficiency in the ob gene behave? (hint: they dont produce leptin) What about after injections of leptin?

A

Act as if they are starved and eat all the time and become obese

Reversed the effects

20
Q

Where is the ob gene expressed?

A

Adipoctyes

21
Q

What effect does starvation have on the body temp, food intake, energey expenditure, immune function, and reproduction?

A

decreased body temp, increased food intake, decreased energey expenditure, decreased immune function, and infertility

22
Q

What doe the db gene encode? where is it expressed?

A

The leptin receptor, hypothalamus with splice variants in other tissues (endothelial cells help leptin cross the BBB)

23
Q

What neurons produce orexigenic effectors?

A

AgRP neurons (hypothalamus)

24
Q

What neurons produce anorexigenic effectors?

A

POMC neurons (hypothalamus)

25
Q

What branch of the nervous system does orexigenic effectors and anorexigenic effectors act on?

A

sympathetic

26
Q

Name the models of regulatory failure causing obesity?

A

failure to produce leptin
low leptin secretions
leptin resistance

27
Q

What is cholecystokinin?

A

satiety signal peptide hormone (short-duration, meal-related)
acts indirectly on the brain
released from GI

28
Q

What is ghrelin?

A

appetite-stimulating peptide hormone (released by empty stomach)
receptor is on hypothalamic AgRP neurons

29
Q

What is PYY?

A

appetite-suppressing peptide hormone (from distal gut: high between meals, medium-duration)

30
Q

Insulin and leptin decrease appetite

A

they simulate anorexigenic effectors

they inhibit orexigenic effectors

31
Q

What are the 5 main energy expenditures?

A

(1) resting energy expenditure (REE) or basal metabolic rate (BMR)
(2) energy expended in digesting, metabolizing, and storing food
(3) volitional exercise: both mechanical work and thermic effect
(4) nonexercise activity thermogenesis (NEAT, e.g., walking to work, typing, etc.)
(5) adaptive thermogenesis

32
Q

What protein in brown fat uncouples the ETC?

A

UCP1 (uncoupler protein 1)

33
Q

What are beige fat cells?

A

White adipose tissue that has been partially converted to brown fat (increased mito and increased UCP1)

34
Q

Where is brown fat found?

A

neck, also more in the young and in women

35
Q

How is UCP1 regulated?

A

transcription (thyroid hormone receptor, beta3 adrenergic receptors, nuclear receptors like PPARgamma and retinoic acid receptor)

cold and overfeeding

nontransciptional regulation also occurs (free FAs active UCP1)

36
Q

What protein causes muscle proton leak?

A

Adenine nucleotide translocase (ANT)

37
Q

What genes have been shown to cause obesity if they are mutated?

A

FTO (gain of function caused obesity), KSR2(loss of function causes obesity),

38
Q

How does KSR2 mediate fat buring?

A

It activates AMPK which tiggers fat oxidation, glucose oxidation, and decreased fat syn.

39
Q

Why are anti-obesity drugs withdrawn?

A

serious sideffects the only FDA approved one is Qsymia

U6 MCP (26 decks)

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