Obesity 1 - CB Flashcards
What BMI is considered underweight?
<18.5
What BMI is considered normal?
18.5-24.9
What BMI is considered overweight?
25-29.9
What BMI is considered grade 1 obese?
30-34.9
What BMI is considered grade 2 obese?
35-39.9
What BMI is considered grade 3 obese?
> 40
Why is BMI imperfect?
doesnt account for sex or racial differences, fat to muscle ratio, or visceral vs subcutaneous fat
how do you measure regional adioposity?
waist to hip ratio (normal females <1.0) and waste to height ratio
skin fold thickness
Risks of being fat:
developing type 2 DM
cardiovascular disease
joint disease, gallbladder disease, reproductive disorders, obstructive sleep apnea, some cancers (hematological, pancreatic, prostate, postmenopausal breast)
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
This costs the US so much money in health care (But it makes us money yay fat people!!!!)
Causes of obesity:
Genetics: polygenic mostly
environment: bad diet, lack of excercise
Gut Microflora
number of adipocytes established early in life
Fact: It appears the biological system seems to be resistant to long term weight changes.
so “the biggest looser” show is a hoax
What is lipostat? what must a lipostat have?
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
What is the fat to brain signaling system? What are the parts to it (signal, sensor, effectors)?
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
True or False: the circulating leptin levels are proportional to the fat accumulation.
True
What mediates leptin levels? what does increased leptin cause? decreased? Stable?
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
What happens to leptin in longterm weight gain?
The “set point” level of leptin is increased causing obesity, but food intake will eventually equal the energy expenditure at the new obese weight
What happens to the sensitivity of leptin in obese people?
it decreases, the lipostat system “defends” the obese state. in general lipostat tries to maintain a constant weight
How do mice with a homozyous deficiency in the ob gene behave? (hint: they dont produce leptin) What about after injections of leptin?
Act as if they are starved and eat all the time and become obese
Reversed the effects
Where is the ob gene expressed?
Adipoctyes
What effect does starvation have on the body temp, food intake, energey expenditure, immune function, and reproduction?
decreased body temp, increased food intake, decreased energey expenditure, decreased immune function, and infertility
What doe the db gene encode? where is it expressed?
The leptin receptor, hypothalamus with splice variants in other tissues (endothelial cells help leptin cross the BBB)
What neurons produce orexigenic effectors?
AgRP neurons (hypothalamus)
What neurons produce anorexigenic effectors?
POMC neurons (hypothalamus)
What branch of the nervous system does orexigenic effectors and anorexigenic effectors act on?
sympathetic
Name the models of regulatory failure causing obesity?
failure to produce leptin
low leptin secretions
leptin resistance
What is cholecystokinin?
satiety signal peptide hormone (short-duration, meal-related)
acts indirectly on the brain
released from GI
What is ghrelin?
appetite-stimulating peptide hormone (released by empty stomach)
receptor is on hypothalamic AgRP neurons
What is PYY?
appetite-suppressing peptide hormone (from distal gut: high between meals, medium-duration)
Insulin and leptin decrease appetite
they simulate anorexigenic effectors
they inhibit orexigenic effectors
What are the 5 main energy expenditures?
(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
What protein in brown fat uncouples the ETC?
UCP1 (uncoupler protein 1)
What are beige fat cells?
White adipose tissue that has been partially converted to brown fat (increased mito and increased UCP1)
Where is brown fat found?
neck, also more in the young and in women
How is UCP1 regulated?
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)
What protein causes muscle proton leak?
Adenine nucleotide translocase (ANT)
What genes have been shown to cause obesity if they are mutated?
FTO (gain of function caused obesity), KSR2(loss of function causes obesity),
How does KSR2 mediate fat buring?
It activates AMPK which tiggers fat oxidation, glucose oxidation, and decreased fat syn.
Why are anti-obesity drugs withdrawn?
serious sideffects the only FDA approved one is Qsymia
