Study found that mice can control the enzyme of lipolysis - fat, research - pharmaceutical industry

U.S. researchers have discovered a new enzyme, break down fat in the control to play the role of higher than expected. Researchers at the January 11 issue of "Nature Medicine" magazine reported that mice with this enzyme, either eat high fat food, or lack of appetite suppressants Hormone It can maintain a slim body.

University of California, Berkeley, professor of nutrition and toxicology Xuehui Shu (sound) that a newly discovered fat cell enzyme, fat metabolism and body weight is an important regulator for the treatment of human obesity will become a full course of promising target.

Control of fat metabolism in the new hero Remarkable is that the fat-specific phospholipase A2 (AdPLA) only exists in the fat tissue a lot. Ad Juan PLA can trigger a series of reactions, thus increasing the called prostaglandin E2 (PGE2) signaling molecule level, while PGE2 inhibits the decomposition of fat.

Not AdPLA mice with low levels of PGE2, fat metabolism rate. The researchers said the lack AdPLA when PGE2 levels decline, the fat decomposition process is not inhibited, even in mice kept eating all day can still stay slim.

In the study, researchers removed the gene expression of Ad Juan PLA mice and normal mice in the control group for comparison. Mice weaned at 3 weeks 1, the researchers began to two groups of mice delicious, high-fat cafeteria. It is noteworthy that this enzyme does not appear to affect appetite, because the two groups of mice to eat as much.

However, as the mice grew up, body weight difference becomes obvious. To 64 weeks, the missing enzyme in mice AdPLA average only 39.1 grams, this low-fat food consumption in mice with the typical body weight is similar to the control group the average body weight of mice up to 73.7 grams. The 64 weeks is considered the laboratory mouse has been to old age. The researchers pointed out, AdPLA loss did not change the number of fat cells, but not for accumulation of excess fat cells.

Researchers also studied whether it can prevent the loss AdPLA genetic obesity in mice. They lack leptin and leptin in mice and the mice lack AdPLA comparison, leptin is a signal to issue the body has been fed hormones. Results only in mice lacking leptin behave like a greedy diners a day than two to three times normal mice eat the food, and soon they become plump up.

Normal circumstances, normal mice daily food intake of 2 grams to 3 grams. In the study, only mice lacking leptin ate 5 grams per day of food, 17 weeks, weight 75 grams, in contrast to the lack of leptin and AdPLA mice every day ate 7.5 grams, 17 weeks, still only 35 grams of weight.

Researchers found that after eating AdPLA increase the value of lipolysis can prevent, reduce fasting AdPLA make more efficient the process of lipolysis. They also found that obese mice AdPLA higher values.

Fat consumption are no longer reach the blood Researchers say, which means that the local signal in adipose tissue allows fat cells directly regulate the body's energy supply, it changed the way people how to regulate the body's basic understanding of fat decomposition. Found, AdPLA deficient mice than normal mice consume more energy, but also directly in the fat cells burn more fat.

The previous assumption that control fat metabolism and body weight of the main characters are endocrine factors, mainly by the different organs and glands secrete hormones, adipose tissue through the blood to reach.

New research results show that in most of the actual behavior of adipose tissue, mainly through PGE2 autocrine and paracrine, in a cell or a group of cells occurred within the field.

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