New Mechanism Halts Fat Production After Eating, Could Treat Obesity

The team's findings could help open doors on research for therapeutic treatment options.
Fabienne Lang

A new, previously unknown, mechanism that plays an integral part in regulating fat production in our body has been found to switch off hours after we eat, as per a new study. 

Scientists from the University of Illinois Urbana-Champaign discovered that the mechanism is abnormal in obese people, and those suffering from non-alcoholic fatty liver disease. 

The study was published in Nature Communications on Tuesday.

What the team discovered about obesity

After eating, our body kickstarts its metabolic system, one part of which involves the pancreas, which produces insulin, which in turn triggers the liver to convert food into fat for our body to store — this process is called lipogenesis.

The process that comes a few hours after we've eaten is what has been previously unknown — until now. 

The study, led by molecular and integrative physiology professor at the University of Illinois Urbana-ChampaignJongsook Kim Kemper, discovered that the gut hormone found in mice, FGF15, known as FGF19 in humans, switched off fat-production in the liver. 

"This gut hormone actually acts as a breaker of insulin action, and specifically inhibits lipogenesis in the liver so that it’s tightly regulated," Kemper said

"For example, with the holidays coming up, if you eat some cookies, the body will release insulin, which promotes lipogenesis. If lipogenesis is not reduced later when the body enters the fasting state, excess fat will accumulate in the liver, so the FGF19 hormone puts the brakes on fat production," she continued.

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The team carried out further tests on mice with obesity and human patients with non-alcoholic fatty liver disease, and discovered that this pathway was abnormal. The gut hormone was highly ineffective in lowering the gene activity needed to turn off lipogenesis, reports News Atlas.

The discovery is a significant one to better understanding this mechanism. "It adds to our understanding of obesity, nonalcoholic fatty liver disease and other metabolic disorders. It also could have implications for other diseases such as diabetes or certain cancers, for which obesity is a risk factor," Kemper explained

"Based on this study, we potentially could search for therapeutic treatment options to target this pathway and increase regulatory function."

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