Fat That Wraps Around Liver, Intestines Is Worse Than Belly Fat: Report

Fat around the liver and intestines is worse than belly fat, a new report has revealed.

For years, scientists have known that visceral fat, or the fat that surrounds the internal organs, has more serious health effects than the subcutaneous fat found underneath the skin, as it has been linked to insulin resistance and inflammation.

This does not mean, however, that subcutaneous fat, which is found in the thighs, rear and belly, is not without negative health implications. Previous research has shown that having belly fat is deadlier than having a higher body mass index.

How exactly does visceral fat affect inflammation and insulin resistance seen in metabolic diseases?

Researchers from the University of Illinois at Chicago (UIC) said that the answer lies in a molecule known as TRIP-Br2.

In their past studies, assistant professor of physiology and biophysics in the UIC College of Medicine Chong Wee Liew and his team have found that among obese individuals, the TRIP-Br2 molecule can only be found in the visceral fat and not in subcutaneous fat.

In a mice study, the researchers were able to prove that mice without the molecule would stay lean and not develop inflammation and insulin resistance.

Liew believes TRIP-Br2 functions by blocking normal fat degradation or lipolysis in cells, causing excess fat to build up.

"Without TRIP-Br2, lipolysis and oxidative metabolism take place at an increased rate, so fat is broken down and quickly used as energy and does not have a chance to build up in organs like the liver," Liew said.

Why is the TRIP-Br2 molecule only present in visceral fat?

Although the overall mechanism is unclear, the researchers concluded that overeating causes the endoplasmic reticulum (ER) to undergo stress. A strained ER in visceral fat eventually produces inflammatory molecules or cytokines. They observed that without the TRIP-Br2 molecule in the visceral fat, stressed ERs do not produce the inflammatory molecules.

Increasing the number of TRIP-Br2 seems to be regulated by intermediary factor GATA3, which Liew said could be a valuable target for the development of therapeutic drugs for obesity.

The study was published in Nature Communications on April 25.

Photo: Tony Alter | Flickr

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