PSYC 370 Lecture Notes - Lecture 11: Cholecystokinin, Genetic Disorder, Serotonergic

• School: Queen's University
• Department: Psychology
• Course: PSYC 370
• Professor: Janet L Menard

Document Summary

Bilateral lesions produce hyperphagia (excessive eating) and extreme obesity. Rats with lesions are very very fat. Classic interpretation- vmh is the (cid:271)rai(cid:374)"s satiety (cid:272)e(cid:374)ter. Postoperative hyperphagia and obesity (what do these rats look like 6m later?: dynamic phase: hyperphagia & rapid weight gain. Begins with a small loss of body weight: static phase: consumption gradually declines to a level just sufficient to maintain stable level of obesity. Shoot way up, then 13 days after surgery, diet decreases but plateaus higher than hc. Animal maintains its new overweight body weight (if rat is deprived of food until losing substantial amount of weight, it regains the lost weight once food deprivation ends, and vice versa) Suggests satiety is still intact, just at a different point. Increases lipogenesis- excess sugar in liver gets turned into adipose fat. Decreases lipolysis: a(cid:374)i(cid:373)al (cid:862)stu(cid:272)k(cid:863) i(cid:374) a(cid:271)sorptive phase. Has to eat more to meet immediate energy needs because sugar gets turned into fat too quickly.