Mouse Genetics of Obesity | Medical-Weight-Loss-Guide.com

The initial research discovering "fat genes" was done on mouse genetics. Some of these mice genes have similar counterparts in humans. Others have only been found to be part of mouse genetics and not part of human genetics. Most of the genes discussed here cause the mice to eat more and to burn fewer calories.

The ob gene encodes for a protein called leptin. Leptin is made by fat cells. When levels are high in the mouse, its brain is signaled to decrease the amount of food it eats and increase the amount of calories it burns.

Additional side effects of the ob gene mutation are low thyroid levels and lack of ability to grow properly. These effects have not been found to occur in humans.

The cell receptor for leptin in the brain is made by the db gene. Mice with this gene do not sense the leptin signal. Therefore, even when large amounts of fat produce high levels of leptin, the mice's brains do not react to it.

Proopiomelanocortin ( POMC ) is a pro hormone which means it is cut into smaller parts that are active hormones. Enzymes change POMC into a-MSH (or alpha-MSH). a-MSH inhibits appetite in the hypothalamus. A defect in the POMC gene leads to increased appetite.

The tub gene encodes a protein made in the hypothalamus. The function of this protein is not exactly know, but defects in it cause obesity in mice.

A gene called fat produces an enzyme called carboxypeptidase E which cuts other proteins into smaller ones. These protein fragments act as signals for different functions. A mutation in the fat gene can cause obesity. This is similar to defects in the PC-1 gene in humans.

AgRP blocks a-MSH's action on MC4R. a-MSH signals the mouse (and human) brain to decrease appetite. If too much AgRP is made, then the a-MSH signal is blocked and the mouse become obese.

Several of the discoveries in mouse genetics have shed light on our understanding of the human genetics of obesity. Not every gene studied is present in humans. These pioneering researchers have laid the groundwork for the discovery for human obesity genes, and they continue to do so.

In mice genetically engineered to be obese, there was a 10 fold increase in the amount of agouti-related expressed DNA. Agouti-related protein (AGRP) blocks MC4R repectors. The mouse mahogany gene plays a role in the signaling from AGRP. It may either bring AGRP to the MC4R repector or hold onto and hide the signals that activate MC4R. Alternativly, turning on the mahogany receptor could activate cellular signals that dampen the MC4R cellular signals.

It is important you discuss any weight loss or exercise plan with your doctor. Only you and your physician can decide what is best for you. Some people have certain conditions that prevent them from doing all exercises, and goal body weights may be different for different people. You need to discuss all these things with your physician before starting any weight loss or exercise program.