One key gut hormone released a few hours after eating, turns off fat production by regulating gene expression in the liver and this regulation is abnormal in obesity, according to a new study.
The researchers from the University of Illinois (UI) found that the gut hormone FGF15 in mice and its human counterpart FGF19 turn off fat-producing genes in the liver.
The hormones are released a few hours after eating when the body transitions from feeding to fasting.
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FGF15/19 activates regulatory molecules to enter the nucleus, the center of the cell where DNA is stored and inhibits gene expression, reports Xinhua news agency.
“This gut hormone actually acts as a breaker of insulin action, and specifically inhibits lipogenesis in the liver so that it is tightly regulated,” said UI molecular and integrative physiology Professor Jongsook Kim Kemper in the study published in the journal Nature Communications.
“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.”
Furthermore, in experiments involving mice with obesity and human patients with nonalcoholic fatty liver disease, the researchers found that the pathway for turning off fat production was dysregulated.
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The genes that the gut hormone regulates were highly active, the FGF15/19-activated regulatory molecules did not even enter the cell’s nucleus and the suppression markers were not added to the genes.
“This study could be very important for understanding this pathway and investigating how it is abnormal in obesity and nonalcoholic fatty liver disease,” Kemper said.
“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.
“Based on this study, we potentially could search for therapeutic treatment options to target this pathway and increase regulatory function.” (IANS)