Obesity Switch
Scientists have discovered an enzyme in mice, the "shutdown" of which by genetic engineering allowed the animals to maintain a normal weight, despite the fact that they ate food with a high fat content and were genetically predisposed to obesity, according to an article published on the website of the journal Nature Medicine.
"We have discovered a new enzyme in fat cells, which is a key regulator of fat metabolism and body weight, having discovered promising ways to find remedies for the treatment of obesity," says the lead author of the study, professor at the University of Berkeley in California, Hei Sook Sul. His words are quoted in the university's message.
The authors of the article discovered an enzyme – adipose tissue–specific phospholipase A2 (AdPLA) - which triggers a chain of processes that increase the number of prostaglandin E2 (PGE2) molecules. This hormone suppresses the breakdown of fat.
In the experiment, mice that had the gene responsible for the production of AdPLA "turned off" were compared with a control group of normal mice.
At the age of about three weeks, all mice were given an unlimited amount of very fatty and delicious food. The presence or absence of the enzyme did not affect appetite, since both groups of animals ate the same amount of food. However, as the mice matured, the discrepancies in the rate of weight gain became apparent.
At the age of 64 weeks – the age of the onset of aging in laboratory mice – animals deprived of the enzyme AdPLA weighed an average of 39.1 grams (weight typical for mice on a low-fat diet), while control mice weighed almost twice as much – 73.7 grams.
The scientists also tested whether the absence of AdPLA could prevent genetically determined obesity in mice.
They compared mice that lacked the hormone leptin, which is responsible for the feeling of satiety, with animals that did not have both leptin and the enzyme AdPLA. Mice with leptin deficiency are extremely voracious, eat two to three times more food per day than normal mice, and they develop obesity very quickly.
In the experiment, "leptin-free" mice ate an average of 5 grams of food per day, while mice that lacked both leptin and the enzyme AdPLA ate 7.5 grams. Normal mice eat an average of 2-3 grams of food per day. At the age of 17 weeks, mice from the first group weighed 75 grams, while rodents from the second group weighed less than 35 grams.
The researchers found that the level of the enzyme AdPLA increased after eating, preventing the breakdown of fat, and decreased during fasting, contributing to the breakdown of fat. They also found that AdPLA levels were higher in obese mice.
Previously, scientists believed that the main role in the management of fat metabolism is played by the endocrine system, primarily hormones. A new study shows that substances in the adipose tissue itself are involved in the regulation of the process.
The authors of the study warn that previous discoveries concerning fat metabolism and appetite regulation in mice have not always been successfully transferred to the human body. Although some people also have mutations in the genes encoding the AdPLA enzyme, the effect of this mutation on humans has yet to be investigated. However, the discovery of the effect of the AdPLA enzyme on fat metabolism may help to discover new methods of combating obesity.
Portal "Eternal youth" www.vechnayamolodost.ru12.01.2009