In fact, the cHF+F+PIO treatment resulted not only in the lowest plasma triacylglycerol levels, but also fully prevented the cHF-induced hepatic steatosis, suggesting that (i) the hypolipidaemic effect resulted from the modulation of hepatic lipid metabolism, including the depression of VLDL-triacylglycerols formation, and (ii) the hepatic effects were mediated by AMP-activated protein kinase (AMPK), stimulated by adiponectin. This evidence concerns the gene ADIPOQ and fatty liver disease.