These findings suggest therapies that decrease the levels of Adgrf1 may help to stop too much fat accumulating in the liver of human patients who are at risk of developing NAFLD.

Treating mice with high levels of liver fat with molecules that inhibit Scd1 decreased the symptoms of Adgrf1-mediated fatty liver disease. A technique called RNA sequencing revealed that Adgrf1 induces expression of enzymes involved in fat synthesis, including a key regulator called Scd1. On the other hand, livers with lower levels of Adgrf1 exhibited reduced fat levels.

The experiments showed that elevated levels of Adgrf1 in human and mouse livers led to increased fat accumulation. studied obese mice and human patients with NAFLD. To investigate the function of Adgrf1 in the liver, Wu et al. Previous studies identified a GPCR known as Adgrf1 that is mainly found in liver cells, but its role remained unclear.

By identifying the GPCRs specifically involved in liver fat accumulation, new treatments for NFALD could be identified. Therefore, a better understanding of NFALD is required to help to develop new strategies for diagnosing and treating the progression of this disease.Ī family of proteins known as GPCRs have crucial roles in regulating various bodily processes and are therefore commonly targeted for the treatment of disease. Instead, only medications which help to manage the associated health complications are available. NAFLD is a major global health issue affecting about 25% of the world's population and, if left untreated, can lead to liver inflammation as well as serious complications such as type 2 diabetes, heart disease, and liver cancer.Ĭurrently, there are no medications which specifically treat NFALD. Being overweight or obese increases the risk of developing numerous medical conditions including non-alcoholic fatty liver disease (NAFLD), where excess fat accumulates in the liver.

Brain test 2 tom level 14