As reaction to elevated plasma triglycerides (TGs) and liver steatosis, hepatic miR-27b was increased, and the ANGPTL3 and GPAM protein were repressed. As reaction to hypertriglyceridaemia and hepatic steatosis, hepatic miR-27b increases, leading to an inhibition of de novo biosynthesis of TGs. Here, GPAM is linked to hypertriglyceridemia.