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Nonalcoholic fatty liver disease (NAFLD) is one of the most common disorders globally, and a leading cause of death worldwide. It is known that NAFLD seems to be more common among men than women. But it is not entirely clear as to why women, especially premenopausal women, are more resistant to this condition than men. Researchers from Pusan National University, Korea, have the answer now.
Through experiments on mice, they have discovered that females produce more of a protein that has a protective effect against nonalcoholic fatty liver disease. It is the formyl peptide receptor 2 (FPR2), the protein that is known to play an important role in mediating inflammatory responses in multiple organs.
The researcher hope that their findings, already published in the journal Nature Communications, could lead to new therapeutic strategies for treating NAFLD.
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Nonalcoholic steatohepatitis (NASH), a progressive form of NAFLD, affects about 30 per cent of all NAFLD patients, and it can lead to cirrhosis and liver cancer. Unfortunately, there is lack of an effective treatment as scientists still do not understand the underlying mechanisms of NAFLD/NASH.
In terms of the gender differences in NAFLD prevalence and severity, current evidence suggests that the sex hormone estrogen plays a protective role in women. The Pusan National University study is the first to determine the role of FPR2 in NAFLD/NASH.
In their study, the researchers found that this protein was highly expressed in healthy livers of female mice. Moreover, they observed FPR2 expressed differently in the livers of male and female mice that were fed a special NAFLD-inducing diet. When they silenced the FPR2 gene, the male and female mice become equally vulnerable to NAFLD, which suggested that FPR2 has a protective effect on the liver.
The research team also came to know that FPR2 production in the liver is mediated by estrogen. They found that male mice that were supplemented with external estrogen produced more FPR2 and were more resistant to NAFLD, whereas female mice that had their ovaries removed exhibited reduced liver FPR2 levels.
Based on their findings, Professor Youngmi Jung, who led the research team, suggested that FPR2 could be a potential therapeutic target for developing pharmacological agents to treat NAFLD/NASH. He is also hopeful the study results could help in the development of gender-based therapies for NASH.
Nonalcoholic fatty liver disease (NAFLD) is a range of conditions caused by the build-up of extra fat in the liver that is not caused by alcohol.
NAFLD is a silent disease with few or no symptoms. If you do have symptoms, we may feel tired (fatigue) or experience pain or discomfort in the upper right abdomen.
Some NAFLD patients can develop nonalcoholic steatohepatitis (NASH), which is marked by liver inflammation and may progress to advanced scarring (cirrhosis) and liver failure. Signs and symptoms of NASH and cirrhosis may include: abdominal swelling (ascites), enlarged blood vessels just beneath the skin's surface, enlarged spleen, red palms, and yellowing of the skin and eyes (jaundice).