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Lecture 7: Control of eating

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What was the problem with the staple stomach way to reduce stomach size and intake? (used to treat morbidly obese)
staples could pop b/c stomach stretched to limit--> leaves a hole leading inner sanctuary to outside world. could lead to an infection
Ok so if this wasn't so how, talk about the gastric balloon attempt.
ehh..this works well for a couple months--makes you feel full
PROBLEM: GI tract will adapt to the balloon by growing-->so they have to inflate balloon more or put in a new one. these only work for 3 months.
What in the stomach stimulates the brain when the stomach stretches?
vagas nerve
OKKK then what about gastric banding?
put a band around stomach constricts stomach and decreases intake (cant expand as much)
PROBL stomach grows: better, but still flawed
What are the problems with GI surgeries?
1) malabsorptive operations are most effective BUT carry greater riske for nutritional deficiencies.
-nausea most common effect
-high risks of osteoperosis and bone disease
-absorption of fat soluble vitamins A, D, E and K are impaired
-dumping syndrome
(causes nausea, weakness, sweating, faintness, and diarrhea after eating)
2) rapid weight loss causes gall stones b/c if decrease intake you decrease signal to gallbladder to release bile to intestinal lumen. so bile just sits there
NOT SMARTEST WAY TO COPE WITH OBEISITY
what's the most sophisticated way to lose weight
reciever stimulates vagus and makes u feel full
Gastric surgery should be used only for morbidly obese, but is this permanent?
yes
avg weight loss is around
15%
Theories of why we eat: Describe the Blood glucose hypothesis
when the difference b/w blood-glucose levels in veins and arteries is low, then we get hungry.
What is the problem with this blood glucose hypothesis?
1)diabetes (high blookd glucose but theyre still hungry
What's a solution to this problem?
Glucostatic theory--glucose utilization-whether or not glucose is getting into the cell or not (thats why diabetics are hungry lots)
What's the problem with the glucostatic hypothesis?
anticipation of eating releases insulin which leads to increase of utilization of glucose so this should make you satiated before even beginning a meal but this obviously doenst happen
Where do most scientists look to explain why we eat?
brain (hypotalamus): VMH and LH
What does lesioning (zapping) and stimulations of the VMH lead to?
lesions- overeating and obesity
stimulations- anorexia, wasting
LH
lesions: anorexia and wasting
stimulations: overeating and obesity

VMH AND LH PLAY LARGE ROLE IN LOTS OF THINGS

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