Uitschakeling enzym voorkomt dik
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Researchers at the University of
California, Berkeley, have identified a new enzyme that plays a far more important role
than expected in controlling the breakdown of fat. In a new study to be published Jan. 11
in the journal Nature Medicine, researchers report that mice that have had this enzyme
disabled remained lean despite eating a high-fat diet and losing a hormone that suppresses
appetite. "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," said Hei Sook Sul, UC Berkeley professor of nutritional
sciences and toxicology and principal investigator of the research. Sul's research
team includes the three co-lead authors of the paper, all from UC Berkeley's Department of
Nutritional Sciences and Toxicology: Kathy Jaworski, former post-doctoral researcher;
Maryam Ahmadian, graduate student; and Robin Duncan, post-doctoral fellow. The enzyme in
the spotlight, adipose-specific phospholipase A2 (AdPLA), is found in abundance only in
fat tissue. AdPLA sets off a chain of events that increases levels of a signaling molecule
called prostaglandin E2 (PGE2), which suppresses the breakdown of fat. Mice that have no
AdPLA have lower PGE2 levels and a higher rate of fat metabolism. "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," said co-lead author
Duncan. In the study, mice that had the gene for AdPLA expression knocked out were
compared with a control group of normal mice. As soon as the mice were weaned at about 3
weeks of age, researchers began offering the two groups of mice an all-you-can-eat buffet
of tasty, high-fat foods.
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