An article published in ‘The Cell’ by researchers from Cincinnati Children's Hospital Medical Center in Ohio, identified that cdk4 protein triggers the development of NAFLD (non-alcoholic fatty liver disease) which occurs at higher levels in mouse models and human patients with the disease. Also, when they blocked the protein in mice, using drugs, it significantly reduced development of hepatic steatosis - the first stage of the disease. NAFLD is the buildup of extra fat in liver cells that is not caused by alcohol. It is normal for the liver to contain some fat, but if 5-10 percent of its weight is fat, then it is classified as fatty liver.

Senior author Nikolai Timchenko, (Professor in the Department of Surgery at the University of Cincinnati and head of the Liver Tumor Biology Program at Cincinnati) and colleagues found high levels of a protein called cdk4 - which is triggered by a high-fat diet - in mouse models of NAFLD and in human patients with fatty liver.

The team also found that blocking cdk4 disrupted the pathways and prevented the development of hepatic steatosis in mice that would normally develop the disease when raised on a high-fat diet, and inhibition of cdk4 in mouse livers with existing steatosis reversed the steatosis. This study thus reveals that activation of cdk4 triggers NAFLD and that inhibitors of cdk4 may be used for the prevention/ treatment of NAFLD.

Read More