What short-term signals turn on feeding behavior? What...

Name: Problem 5, Chapter 8: Quantitative Human Physiology
Uploaded: 2021-04-27T15:50:47-08:00
Duration: 1 min 28 s
Channel: Katie Haasch
Description: What short-term signals turn on feeding behavior? What short-term signals turn off feeding behavior? What is GLP-1? Where is it made? What increases its secretion? What is ghrelin? Where is it secreted? What stimulates its secretion?

What short-term signals turn on feeding behavior? What short-term signals turn off feeding behavior? What is GLP-1? Where is it made? What increases its secretion? What is ghrelin? Where is it secreted? What stimulates its secretion?

Key Concepts

GLP-1

Glucagon-like peptide 1 (GLP-1) is an incretin hormone that plays a role in reducing food intake and enhancing insulin secretion. It is primarily produced by the L-cells located in the intestinal lining, particularly in the distal small intestine and colon. Its secretion is stimulated by the presence of nutrients, notably carbohydrates and fats, in the gut, thus contributing to postprandial satiety and glucose regulation.

Orexigenic Signals

These are short-term signals that stimulate feeding behavior by indicating energy insufficiency. They typically increase during fasting states and signal the brain to initiate hunger. A key example of an orexigenic signal is ghrelin, which is released when the body requires energy, thus promoting food intake.

Anorexigenic Signals

These signals work on the short-term regulation of feeding behavior by promoting satiety and reducing appetite. They are released during and after food intake and contribute to the cessation of eating. Hormones like GLP-1, CCK, and PYY serve as anorexigenic signals by communicating nutrient availability to the brain, thereby helping to terminate meals.

Ghrelin

Ghrelin is an orexigenic hormone that promotes hunger and food intake. It is mainly secreted by specialized cells in the stomach, specifically in the gastric fundus, and to a lesser extent by other tissues. Its levels rise during periods of fasting and are influenced by low nutrient availability, acting as a critical signal to the brain to initiate feeding behavior.

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