CHICAGO, Nov. 7 (Xinhua) -- A study led by the University of Michigan (UM) found that increasing the levels of the fat hormone Neuregulin 4 (Nrg4) protected liver cells from metabolic stress in mice, while loss of the hormone had the opposite effect: mouse livers deteriorated and progressed to nonalcoholic steatohepatitis (NASH) more quickly.
UM cell biologist Jiandie Lin and his colleagues evaluated the effects of Nrg4 in mice that had been fed the type of high-fat, high-sugar diet that leads to fatty liver disease.
The findings have been published in the latest issue of the Journal of Clinical Investigation.
They found that when the hormone was elevated, less cell death, less inflammation, less fibrosis were detected.
On the other hand, mice lacking the hormone fare much worse. The hormone is having a distinct function that limits cell death and prevents progression to the most severe fatty liver disease.
More than a third of U.S. adults and up to 10 percent of children have some form of fatty liver disease. In up to 20 percent of these patients, the liver cells begin dying, and the disease develops into NASH.
It is estimated that by 2020, NASH will become the leading cause of the need for liver transplants, surpassing hepatitis and alcoholic liver disease.
The findings are an expansion of a previous study from Lin's lab, which showed Nrg4 could prevent the liver from converting sugar into fat, lowering the risk of fatty liver disease at its outset.
Moreover, the researchers have not yet seen any negative side-effects in the mice with increased Nrg4.
Based on the findings, researchers believe that Nrg4 may be an effective target for therapeutic intervention of NASH.
Lin's lab is now focusing on further testing the therapeutic viability of the hormone in treating NASH.