Study Findings on Fatty Liver Disease Detailed by Researchers at Peking University Health Science Center (Ribosomal modification protein rimK-like family member A activates betaine-homocysteine S-methyltransferase 1 to ameliorate hepatic...).

A new report from researchers at Peking University Health Science Center provides fresh data on fatty liver disease. The study focuses on the role of a protein called ribosomal modification protein rimK-like family member A (RIMKLA) in regulating glucose and lipid metabolism. The researchers found that RIMKLA expression was reduced in the livers of humans and mice with nonalcoholic fatty liver disease (NAFLD). They also discovered that RIMKLA is a protein kinase that phosphorylates betaine-homocysteine S-methyltransferase 1 (BHMT1) to repress lipid synthesis and uptake in hepatocytes. The study suggests that inhibiting RIMKLA may promote hepatic lipid deposition. [Extracted from the article]