what is obesity? why does it occur?
intake of more calories than expenditure of food. we are genetically programmed to store fat in order to survive and reproduce. exacerbating factors include lack of physical exercise, plentiful inexpensive food, and caloric imbalance
why is it wrong to define obesity as a disease?
shifts responsibility to physician, not pt. pt. should be stongly motivated to not overeat/overconsume calories
why is there a push for obesity to be categorized as a disease?
so that insurance companies will pay for tx
what is an example of incremental weight gain?
avg. woman in US gains 25 lbs from age 25-65
what is ghrelin?
peptide hormone released by the stomach that affects the hypothalamus, stimulates 2 neuropeptides: Agouti related protein, (AgRp) and Neuropeptide, (NPY, Y stands for tyrosine)
what do Agouti related protein, (AgRp) and Neuropeptide, (NPY) do?
they are orexogenic, stimulate appetite by synthesizing other NTs to go to the GI and affect motility
how can ghrelin levels be regulated?
bariatric sx, reduction of stomach vol, lowers blood ghrelin conc.
what are the 2 main anorexogenic, (appetite decreasing), hormones? where are they made?
insulin from the pancreas, and leptin from adipose tissue
what happens if you destroy the leptin gene? what happens if you inject exogenic leptin into a mouse or a human?
destroy the leptin gene, a mouse will become obese, inject a mouse with exogenic leptin, it will lose weight, though the same result cannot be repeated with humans
where are the receptors for leptin and insulin? what happens when they bind?
they bind to receptors in the hypothalamus, and stimulate anorexogenic NTs such as alpha melanocyte stimulating hormone, (alpha-MSH), (it’s receptors are in the hypothalamus)
where does alpha melanocyte stimulating hormone come from?
Proopiomelanocortin, (POMC), long peptide when cleaved gives a variety of products, including alpha-MSH
what is the action of alpha melanocyte stimulating hormone?
alpha melanocyte stimulating hormone inhibits the action of orexigenic neurotransmitters, Agouti related protein, (AgRp), and Neuropeptide Y, (NPY)
what is PYY, where does it come from, what does it do?
PYY is a hormone produced in the large intestine that inhibites orexigenic signals including the receptor NPY, and signals from the intestines -> stimulated hypothalamus
what is the effect of dopamine and seratonin on appetite?
they cause a decrease in feeding/wt gain
what increases with increased dopamine? what has been associated with low dopamine?
feelings of pleasure. addiction to narcotics, gambling, and overeating are associated with pts in low dopamine
excess of any fuel, including protein will result in?
fat deposition
obesity is associated with metabolic syndrome, which is associated with what 4 conditions?
central obesity, (pear shape), inefficient insulin regulation of carbs, (often diabetes), HTN, (more fat=more pressure on CV), dyslipiemia, (increase in “bad lipids”, cholesterol, LDLs)
what does BMI stand for?
amount of wt per unit of surface
why is no diet ultimately effective?
no diet can work long term
what is the pritikin diet? will you lose weight?
low fat, high carbs, high fruits/vegetables. developed as anti-sclerotic diet, reduce levels of insoluble lipids, (cholesterol, oxidized lipids), which form “fatty streaks” in vasculature, some of which are congential. not intended as a weight loss diet.
what is the atkins diet? what was it designed to do?
high fat, high protein, low->no carbs, pts will lose weight on this diet
b/c the adkins diet cuts out carbs what is necessary to do?
need to supplement w/vitamins
why is the adkins diet effective in promoting weight loss?
it is a hypocaloric diet in disguise, the metabolic products from protein/fat supress appetite
how do high fat and protein levels affect glucagon?
glucagon levels rise, stimulates catabolic processes, (b/c not much glucose)
what did the long term study find out about how the adkins diet affects people over a year?
nontoxic, people live off ketone bodies, no increase in cholesterol/triglycerides. the weight loss will level off with a slight increase at the end.
what was found in mice on the adkins diet in comparison to mice w/typical western diet, and pritikin diet?
adkins diet mice had significant increase in atherosclerosis
what is the south beach diet?
moderate amounts of fats and proteins, emphasis on “good fatty acids”, (no saturated or trans), use carbs with low glycemic index, (reduce insulin “burst”).
excercise is essential.
how does exercise help regulate diet?
AMP regulated protein kinase B increases catabolic processes such as lipolysis, glycogenolysis and decreases anabolic processes such as fatty acid and cholesterol synthesis. excercise makes ADP, 2 of which is converted to 1 ATP and 1 AMP by adenyl kinase -> thus excercise increases AMP conc for protein kinase B
where does resisitance to lose weight come from biologically according to once theory?
genes and the brain try to maintain a set point of weight for the body
what is an example of evidence pertaining to adipocytes for the set weight point theory?
adipocytes can only get so big before their number has to be increased to keep up with input, however, you can never lose adipocytes once you create them.
what are 4 examples of evidence for the set weight point theory?
leptin, insulin conc, ghrelin, free FAs
why is the set weight point situation a problem with childhood obesity?
they will be stuck with the same number of adipocytes for the rest of their life
what is dinitrophenol?
weight loss drug, phosphorylation decoupler, converts food -> heat, eventually fatal
what is fen-phen?
anti obesity drugs, fenfluramine and phentermine, NTs to depress appetite, increase satiety -> can cause heart failure
how do amphetamines help cut weight?
sympathetic amine that stimulates CNS activity, depresses appetite
what is ephedrine?
powerful stimulant which increases thermogenesis via decoupling of oxidative phosphorylation, also associated with heart disease
what is sibutramine?
dopamine and seratonin receptor blocker, good drug, but insignificant weight loss which is only dependent on drug use
what is orlistat?
weight loss drug which is an inhibitor of gastric and pancreatic lipase -> pt cannot digest fats, get oily feces and bloating
what is rimonabant?
canabinoid receptor blocker, developed to help people stop smoking, was also found to reduce obesity. not approved by the FDA
what are 4 major pathological consequences of obesity?
insulin resistance, (related to mult pathways), cardiovascular disease, (peripheral resistance to circulation, high Na+, and increased LDL/VLDL, decreased HDL), pulmonary disease, (breathing rate increases with weight strain/heart rate), and some kinds of CA, (can be gender specific)
what are low risk behaviors for avoiding obesity?
bmi <25, high fiber, polyunsat fatty acids, (needed for prostaglandins/leukotrienes), low trans fats/low glycemic index, mod. physical activity, and no smoking
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