Hunger, Satiety and Obesity

Nov 12, 2012 at 05:05 pm by steve


What Regulates Our Appetite?

Our body naturally tells us when to eat and when to stop by hormones and neurons: ghrelen, neuropeptied Y, cholecystokinin, peptide YY, insulin, leptin and melanocortin. Problems begin when we do not listen to the signaling of our body. As we continue to consume more calories than needed without expending them, we start to develop excess fat and over time this can lead to health problems due to an erroneous message sent by the hormone leptin. Our appetite, hunger and satiety are regulated by the endocrine system that communicates with the hypothalamus and is controlled by a negative feedback system which can be disrupted by an improper diet leading to obesity.

 

The stomach secretes a hunger hormone that sends a message to the brain to tell us it is time to eat. When our stomach is empty it produces the hormone ghrelin. Ghrelin sends a message from the epithelial cells of the gastric fundus to the arcuate nucleus of the hypothalamous, which is the center for appetite regulation in the brain. Ghrelin then stimulates the neuropeptide Y secreting neurons in the brain to increase hunger.

 

Upon consuming food, our stomach stretches and hormones start communicating with the appetite control center to signal satiety. Ghrelin concentrations decrease due to the release of the hormone cholecystokinin (CCK) from the enteroendocrine cells of the small intestine. Cholecystokinin then works together with another hormone called Peptide YY from the large and small intestine in a negative feedback cycle to control the appetite over a period of time.

 

Another hormone that controls our appetite is insulin. Insulin is released from the beta cells of the pancreas to indicate that your body is metabolizing and not to consume anymore food. Insulin regulates our fat stores by stimulating adiposytes (fat cells) to take up glucose and store as fat to use as energy at a later time. As we eat, adiposcytes are stimulated to secrete leptin which stimulates melanocortin secretion in the arcuate nucleus of the hypothalamus signaling satiety, preventing the continued release of neuropeptide Y.

 

Improper diet can lead the accumulation of excess adipose tissue and cause disruption in signaling of leptin secretion. A person with a higher body fat mass will secrete an excess of leptin by the adipose cells. Here is the problem: over a long period of time this excess secretion of leptin can cause a disturbance in our negative feedback system. This causes our feedback system to become unresponsive to leptin or to have a receptor defect on the target cells in the hypothalamus.

 

This disruptive signal of leptin signaling sends a message to the brain that we are hungry even after we just ate a big meal. This could be a contributing factor that leads to obesity and other health disorders like fatty liver and insulin resistance. The best way to these issues is to follow a healthy nutrition plan and exercise.     

 

Resources:

http://www.ncbi.nlm.nih.gov/books/NBK22251/

http://www.jci.org/articles/view/36284

http://www.cdc.gov/pcd/issues/2009/jul/pdf/09_0011.pdf http://circres.ahajournals.org/content/101/6/545.full

 

Robert A. Shaffer MD is the Medical Director of Shaffer Weight Loss Center at Gastroenterology Associates, N.A.P.C.

 

Editor: This article first appeared in the Birmingham Medical News blog.

 

 

 




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