The studies conducted here demonstrate that: 1) injection of ethanol stimulates consumption of a high-fat diet in preference to a low-fat carbohydrate-rich diet; 2) intake of ethanol with fat synergistically raises circulating TG levels; 3) lowering TG levels leads to a reduction in voluntary ethanol intake; and 4) lowering TG levels decreases PFLH OX expression in ethanol-drinking animals. These results lead to the conclusion that manipulation of TG levels, by ingestion of a high-fat meal or administration of a lipid-lowering drug, can impact ethanol consumption via its effect on a hypothalamic peptide that controls ethanol intake. Given the increases in obesity and hypertriglyceridemia in many of the world’s populations in recent years (Ford et al., 2004; Lilja et al., 2008), these findings have potentially important implications, both for the treatment of alcohol addiction as well as for nutritional choices that have medical consequences.
