In a recent study the researchers at University of California, Berkeley could zero onto an enzyme in the adipose tissue by disabling which the mice could remain lean despite being fed a fat diet. Surprisingly, the researchers noted that the disabling of enzyme also resulted in the loss of a hormone that suppresses appetite. The study was published in the January 11th issue of Nature Medicine.
Lead investigator and Professor of nutritional sciences and toxicology at Berkeley University, Hei Sook Sul said "We have discovered a new enzyme within fat cells that is a key regulator of fat metabolism and body weight, making it a promising target in the search for a treatment for human obesity,"
The AdPLA enzyme also known as phospholipase A2, is an enzyme specific to adipose tissue. It is found in large quantity in the fat tissues. AdPLA results in increased production of PGE2 or prostaglandin E2 that contains fat breakdown. The mice that had lower levels of PGE2 had a higher fat-metabolism. Co-author Duncan notes this phenomenon when he quoted "When levels of PGE2 are decreased because of the lack of AdPLA, fat breakdown proceeds unchecked, resulting in leanness even in animals that eat all day long."
The researchers also noted that the enzyme levels did not affect the intake of food or the appetite of the mice as the two groups studied for this research had similar levels of appetite. One of the groups had its AdPLA expression disabled while the other group consisted of normal mice. Both the groups were fed high-fat containing food items for finding the affect of enzyme disablement on the mice. At 64 weeks of age, the mice with disabled enzyme functioning had an average weight of 39.1 gm as compared to average weight of 73.7 grams among the normal group.
It was an important observation made by the researchers that noticed no change in the number of fat cells in both kinds of mice but the mice with missing AdPLA did not store fat and hence the average weight of the mice was far lower.
Further briefing about this study is available at http://www.eurekalert.org/pub_releases/2009-01/uoc–dea010909.php
{ 1 trackback }