American researchers decode cellular regulation behind visceral fat production

Researchers at the University of Illinois may have found two new drug targets to stop visceral fat-forming in obese people.
The Chicago team has made the discovery while studying molecular processes mediating fat accumulation in the body.
The body is carrying two different types of fat and there is a link between its location and metabolic disease risk.
Visceral fat, which wraps around the internal organs, contributes to insulin resistance and inflammation, two driving factors for the development of type 2 diabetes.
The subcutaneous fat that lies just under the skin around the belly, thighs and rear, on the other hand, doesn’t carry the same risks and some of it may even be protective, according to the researchers.
In previous studies, the Illinois team identified in obese participants a novel regulator of fat lipolysis (the breakdown of fat in fat cells) called TRIP-Br2.
They suspected then that the regulatory molecule TRIP-Br2 was produced in response to cellular stress caused by overeating, and that it was found in higher amounts in visceral fat than in subcutaneous fat.
Mice studies done by the Chicago group looked this time at depot-specific differences on a molecular level when TRIP-Br2 was activated in visceral fat.
The animals fed a high calorie diet where TRIP-Br2 was knocked out stayed relatively lean and free from insulin resistance and inflammation, as opposed to the control group where the molecule was active.
The findings – published in the Journal Nature Communications – suggest that when TRIP-Br2 is turned up in visceral fat cells, optimal lipolysis isn’t possible. As a result, excess fat builds up in the cells.
Without TRIP-Br2, however, lipolysis takes place at an increased rate, so much so that fat is used as energy immediately after being broken down and can’t accumulate in the liver.
The absence of TRIP-Br2 is also correlated with reduced inflammation and oxidative stress by indirectly preventing the production of inflammatory molecules known as cytokines.
The down-regulation of TRIP-Br2 in visceral fat cells could be achieved by controlling simultaneously a second intermediary factor the researchers become aware of called GATA3, which they hope one day could be used as targets for drugs against obesity.