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50 Cards in this Set
- Front
- Back
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what are the BMI values
Underweight: Normal: Overweight: Obese Grade I: Obese Grade II: Obese Grade III: |
Underweight: <18.5
Normal: 18.5-24.9 Overweight: 25-29.9 Obese Grade I: 30-34.9 Obese Grade II: 35- 39.9 Obese Grade III: >40 |
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what factors determine a positive energy balance
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more comes in than goes out...
Genetics: polygenic Environment: sedentary, high E foods, fast food, extra sugar, large meal size |
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what is the definition of obesity
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based on relationship btwm BMI and premature death
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what does obesity increase the risk of developing
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DM
HTN Heart Disease Stroke |
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hypertrophy &
hyperplasia of fat cells what TF activates both of these processes |
Hypertrophy: initial weight gain, fat cells get larger
Hyperplasia: more fat cells are made **weight loss will decrease the hypertrophy of fat cells but not the hyperplasia (cant get rid of fat cells) **PPAR gamma |
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what does PPAR gamma do?
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it increases the number and size of fat cells
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what are TZD's
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insulin sensitizing thiazolidinediones used to treat DM II (insulin resistant fat) activate PPAR gamma to get FFA out of circulation and into fat cells. They make ppl gain weight
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what drugs activate PPAR gamma
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TZD's thiazolidinediones
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fat located where will increase the risk of heart disease, DM, HTN
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Abdomen
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moderate weight gain/loss will affect what? hypertrophy or hyperplasia
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hypertrophy
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What is POMC and what does it stimulate
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The arcruate nucleus of the hypothalamus has one set of neurons called POMC which generates aMSH which inhibits apetite and increases E expenditure
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what effect does aMSH have on energy balance?
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- E balance (decrease apetite, increase expenditure)
from POMP neurons of the ARC of the hypothalamus |
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what does the other set of neurons (not POMC) release and what are its effects>
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neuropeptide Y (NPY)
Agouti-related protein (AgRP) stimulate apetite and decrease energt expenditure. reduce fertility |
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what is the effect of NPY and AgRP
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increase apetite
decrease expenditure **positive E balance |
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where do aMSH and NPY/AgRP converge?
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at the satiety center: NTS (nucleus tractus solitarius)
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describe how NEAT ESTABLISHES body weight set point
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neat is genetic and causes lean ppl to be lean and obese ppl to be obese
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what did the experiment with the pima indians suggest
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several famines wiped out skinny ppl and the genetics favored 'thrifty' ppl. BUT the lazy group who ate lots was obese and the hard working group that ate well was skkinny. genes do have an influence BUT enviornment can overcome it
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what is a set point
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its the genetically determined weight you should be. can be overcome by enviornment
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does weight loss trigger a positive or negative energy balance
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POSITIVE:
you get strong hunger signals (hyperphagia) and you decreases RMR increase E intake, decrease E expenditure |
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when you loose weight what does RMR do? will this change last?
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RMR decreases
the RMR will remian at the lower value for as long at the weight is lost **this is kinda shitty today but it worked well in a fammine so that you wont loose more weight |
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will a decrease in RMR minimize weight loss or increase it?
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minimize
when you loose weight your RMR will decrease and prevent further weight loss (evolutionary trick) |
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why does RMR decrease when you loose weigh
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decrease in T3 (thyroid hormone) which will decrease Na/K ATPase activity
Na/K ATP ase uses about 20% of RMR **body can adapt to having a bit more Na in the cell |
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what type of energy balance does weight gain induce
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negative:
satiety centers are activated (decreased hunger) increased RMR and NEAT (increased energy expenditure) |
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so the whole set point thing, what is it more geared towards?
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weight gain, after overeating there may not be a negative energy balance that comes into play and ppl can become over weight and cahnge their 'set point'
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what part of the brain regulates fats
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arcruate nucleus of hypothalamus
**monitors nutrient stores and regulates feeding activity |
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name three molecules associated with feeding and name their location
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Leptin: from fat
Pyy: from intestines Ghrelin: stomach |
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what is the effect of leptin on POMC (aMSH) and NYP/AgRP
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leptin will activate POMC (aMSH) and inhibit NYP/AgRP
**apetite is activated and energt reduction in indiced |
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what is the effect of Pyy
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the stomach sercretes PYY which inhibits NPY so apetite is reduced
**NPY will stimulate apetite and reduce E expenditure BUT Nyy will inhibit its action |
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What is the effect of Ghrelin
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activates NYP/AgRP
**NYP stimulates apetite and decreases energy expenditure |
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what is the biochemical pathway of weight gain (leptin to responses)
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weight gain
increased leptin from fat cells hypothalamus sense leptin this leads to an increase in aMSH which will decrease appetit and increase E expenditure and increases sympathetic tone **what does increased leptin do to NPY? inhibits it (NPY stimulates appetite) |
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what is the biochemical response to weight loss
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leptin is decreased: no release from fat cells
the hypothalamus senses the decrease in leptin NPY/AgRP is increased and responses to starvation ensue increased food intake decreased E expenditure decreased reproduction/temperature increased parasympathetics |
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what hormone is released in response to fasting?
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ghrelin from the stomach acts on NPY to increase apetite and decrease energy expenditure
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what hormone(s) are released in response to a meal?
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saitety signals from the GI
GLP1: decreases appetite by acting on aMSH CCK: secreted in response to fat/AA decreases appetite in NTS satiety center |
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what monitors stomach distension
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vagus N, when distended appetite is supressed
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when your overfed:
what hormones from what tissues and what affect |
Pancreas: insulin
Stomach: no ghrelin Fat: Leptin intestine: CCK/PYY causes a decrease in appetite (aMSH activated, NPY inhibited) |
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what tissues secrete what hormone and what is the effect to starvation/undernourished/fasted
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stomach produces ghrelin to stimulate AgRP/NPY which will stimulate the apetite
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how does the arc work
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area of hypoythalmus that monitors blood to detect nutrient levels
***BBB missing@ hypothalamus |
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what r leptin levels approxamate to?
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adipose levels, it acts on aMSH to inhibit apetite. leptin inhibits AgRP/NPY
**obese ppl are leptin resistant so they dont get the 'stop eating' signal |
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what molecules monitor long/short term nutrient levels
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Short: nutrients in circulation/insulin
Long: leptin |
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is leptin better at preventing weight loss or gain?
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loss
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what does low leptin and low insulin stimulate?
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GOAL: stimulate appetite
inhibit aMSH activate: Ag/RP/NPY |
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what is a monogenic cause of obesity?>
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leptin deficeincy (MC4R)
the body doesnt get the "stop eating, im full of fat" signal that activates aMSH *its rare and it treated with leptin injection |
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when you dont sleep what happens to leptin and ghrelin
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leptin is decreased
ghrelin in increased **you get HUNGRY |
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what hormone does insulin work with, leptin or ghrelin? what will a drop in insulin (IR) do to these hormones?
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leptin (both indicate the body is fed)
*increase aMSH to inhibit apetite *decrease NPY/AgRP to keep apetite low *when IR occurs, it wont be able to inhibit NPY/AgRP so it can make you feel hungry |
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why is polyphagia is one of the three P's of DM
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no insulin, insulin works with leptin to inhibit apetite by activating aMSH and inhibiting AgRP/NYP but when IR is missinf AgRP is active and stimulates hunger
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how does imflammation contribute to obesity?
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adipose has lots of macrophages, these macrophages are proinflammatory
inflammation leads to IR, IR is involved with DMII fatty liver. polycystic ovarian disease, HTN |
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what is more important weight loss or exercise with IR?
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exercise
**exercise independent of weight loss will releieve some of the bad things associated with obesity |
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best weigh to loose weight?
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not a diet, LONG TERM
low cal to loose weight loose 7-10% of body weight to see benefits |
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to maintain weight loss how many calories need to be burned
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Women: 2500
Men: 3300 *per week |
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what are recommendations for loosing weight?
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1.5 hrs of activity/day
low cal diets low fat, high carbs monitor weight be mindful of E density, a huge plate of veggies vs a small cookis for the same # of cal |
