It has long been known that visceral fat it the type of fat more dangerous to our health than subcutaneous fat. Visceral fat wraps around out organs whereas subcutaneous fat lies just beneath the skin – often on the thighs, belly and bottom. Despite this knowledge, it has been somewhat unclear as to how visceral fat increases the risk of insulin resistance and inflammation. It can even increase the risk of death in people with a normal BMI.
A study led by researchers at the University of Illinois at Chicago points blame at a regulatory molecule in cells called TRIP-Br2 that is produced in response to overeating’s stress on the machinery cells use to produce proteins. In previous studies, Chong Wee Liew and his colleagues found that in obese humans TRIP-Br2 was turned-up in visceral fat but not in subcutaneous fat. When the researchers knocked out TRIP-Br2 in mice and fed them a high-calorie, high-fat diet that would make the average rodent pack on the grams, the knockout mice stayed relatively lean and free from insulin resistance and inflammation.
It appears that TRIP-Br2 prevents the break-down of fat to be used as fuel (lipolysis). Lipolysis prevents fat building up within the cells. When the TRIP-Br2 is not present, our metabolisms increase and lipolysis occurs at a faster rate to more efficiently turn the fat into fuel for the body. This prevents it accumulating in and around organs like the liver.
But Liew and his colleagues still didn’t know why TRIP-Br2 was found in higher amounts in visceral fat than in subcutaneous fat. Their search for answers led them to a cellular structure called the endoplasmic reticulum, or ER, which is responsible for producing all the proteins in the cell. Nutrients from a meal enter the ER, but an excess due to overeating can significantly stress it. In obesity, a stressed ER in visceral fat cells leads to production of inflammatory molecules called cytokines – but exactly how was unclear.
The best approach to weight control will always be to follow a healthy balanced diet and to incorporate exercise. We should steer away from quick fixes and focus on these two things that were effective for many decades in the past. Nonetheless, further research will be interesting.
Liew and coworkers found that in the absence of TRIP-Br2, ER stress could no longer trigger cytokine production and inflammation in obesity. They also found that the up-regulation of TRIP-Br2 in visceral fat depends on an intermediary factor called GATA 3 that turns on TRIP-Br2. “Together, our findings indicate that these molecular regulators, TRIP-Br2 and GATA3, could be viable targets for small drug molecules that could serve as potential therapeutic agents against obesity,” Liew said.
More research in this area may lead to a better understanding of the relationship between visceral fat and lifestyle related disease and also methods of weight maintenance and control.
