MEDI211 Lecture Notes - Lecture 3: Fenfluramine, Bariatric Surgery, Junk Food
Week 2 Lecture 3 – When metabolic control dysfunctions
Lecture Objectives:
•To gain understanding of metabolism dysfunctions; characteristics of, contributing
factors, and pathogenesis of weight gain and obesity.
Appetite influencers:
•Insulin and Cholecystokinin (an incretin) influence appetite
•Ghrelin is released when the stomach is empty; when stomach is full its release is inhibited.
•Leptin is released from adipocytes when they are full of lipids; when they are not full the
secretion of leptin is inhibited.
Overweight and obesity:
•Neuropeptide Y (NPY) stimulates food intake and inhibits energy expenditure
•Pro-opiomelanocortin (POMC) inhibits food intake (satiety) and stimulates energy
expenditure.
•Fat stores and insulin affect this pathway —> secretion of insulin activates POMC
•When we don’t have food, we release ghrelin, which stimulates NPY and inhibits POMC.
•Leptin is our satiety hormone —> it stimulates POMC and inhibits NPY.
•
•People with lots of fat stores have lots of leptin, yet this isn’t decreasing their appetite, so
something isn’t working the way it should. Addressing this form a biological perspective, we
live in an obesogenic environment. We have evolved to be able to store a lot of energy for
survival. Our evolutionary preference to conserve positive energy balance makes fat in
the ‘new’ habitat.
Why do the homeostatic controls of body weight fail in so many people?
•There is a theory that constantly being exposed to high simple carbohydrate diets has lead to
resistance to the normal physiological responses.
•Abnormal regulation of brain circuits control appetite/satiety. Eg. Insulin and leptin normally
inhibit NPY, but we now are seeing central resistance to insulin and leptin in obesity.
•Another theory as that we have failing mechanoreceptors in the stomach and oesophagus.
When the stomach stretches, vagal afferent firing to brain tells us we are full. However, these
receptors become less active if they are overworked ie. if we are constantly filling our
stomach.
Gastric Mechanoreceptors:
find more resources at oneclass.com
find more resources at oneclass.com
Document Summary
To gain understanding of metabolism dysfunctions; characteristics of, contributing factors, and pathogenesis of weight gain and obesity. Ghrelin is released when the stomach is empty; when stomach is full its release is inhibited. Leptin is released from adipocytes when they are full of lipids; when they are not full the secretion of leptin is inhibited. Neuropeptide y (npy) stimulates food intake and inhibits energy expenditure. Pro-opiomelanocortin (pomc) inhibits food intake (satiety) and stimulates energy expenditure. Fat stores and insulin affect this pathway > secretion of insulin activates pomc. When we don"t have food, we release ghrelin, which stimulates npy and inhibits pomc. Leptin is our satiety hormone > it stimulates pomc and inhibits npy. People with lots of fat stores have lots of leptin, yet this isn"t decreasing their appetite, so something isn"t working the way it should. Addressing this form a biological perspective, we live in an obesogenic environment.
