Modulation of hepatic steatosis by dietary fatty acids

Abstract

Non-alcoholic fatty liver disease (NAFLD) describes a range of conditions caused by fat deposition within liver cells. Liver fat content reflects the equilibrium between several metabolic pathways involved in triglyceride synthesis and disposal, such as lipolysis in adipose tissue and de novo lipogenesis, triglyceride esterification, fatty acid oxidation and very-low-density lipoprotein synthesis/secretion in hepatic tissue. In particular, it has been demonstrated that hepatic de novo lipogenesis plays a significant role in NAFLD pathogenesis. It is widely known that the fatty acid composition of the diet influences hepatic lipogenesis along with other metabolic pathways. Therefore, dietary fat may not only be involved in the pathogenesis of hepatic steatosis, but may also prevent and/or reverse hepatic fat accumulation. In this review, major data from the literature about the role of some dietary fats as a potential cause of hepatic fat accumulation or as a potential treatment for NAFLD are described. Moreover, biochemical mechanisms responsible for an increase or decrease in hepatic lipid content are critically analyzed. It is noteworthy that both quantitative and qualitative aspects of dietary fat influence triglyceride deposition in the liver. A high-fat diet or the dietary administration of conjugated linoleic acids induced hepatic steatosis. In contrast, supplementation of the diet with krill oil or pine nut oil helped in the prevention and/or in the treatment of steatotic liver. Quite interesting is the “case” of olive oil, since several studies have often provided different and⁄or conflicting results in animal models.

Keywords: Hepatic steatosis; Non-alcoholic fatty liver; Fatty acids; Lipogenesis

Core tip: Dietary fats may not only influence the pathogenesis of liver diseases, but may also prevent and/or reverse their expression. This manuscript reviews the molecular mechanisms responsible for the regulation of hepatic lipogenesis, through which some fatty acids may be beneficial or detrimental to non-alcoholic fatty liver disease (NAFLD). We believe that an understanding of the biochemical mechanisms underlying fat accumulation in the liver will lead to more targeted and effective therapeutics for hepatic steatosis. This is a particularly important topic because NAFLD is an increasingly prevalent disease which, to date, has no proven pharmacologic treatment to prevent or reverse its course.