Author information
1 Yale University, Department of Internal Medicine, 300 Cedar St, PO BOX 208020, New Haven, Connecticut, US.
2 Yale University School of Medicine, 300 Cedar St, New Haven, Connecticut, US.
3 Yale University, Cellular and Molecular Physiology, 300 Cedar St, New Haven, Connecticut, US.
4 Yale University School of Medicine, Department of Internal Medicine, PO Box 208020, New Haven, Connecticut, US.
5 Howard Hughes Medical Institute, Yale University, Department of Internal Medicine, Yale University School of Medicine, P.O. Box 9812, New Haven, Connecticut, US.
Abstract
Nonalcoholic fatty liver disease (NAFLD) and insulin resistance often coincide. These twin epidemics are both sequelae of ectopic lipid accumulation, but the mechanistic links between them are debated. The protein kinase C family of serine/threonine kinases has been implicated in altered insulin action in liver, muscle and fat cells for over three decades and provides a putative link between NAFLD and insulin resistance.