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

Figure 1

Contribution of various metabolic pathways to hepatic steatosis. Liver fat content reflects the equilibrium between several metabolic pathways involved in triglyceride synthesis (red arrows) and clearance (green arrows). Dietary fat is an important factor capable of influencing de novo lipogenesis (black dotted arrow).

Figure 2

Pathway of de novo fatty acid synthesis in the liver. CIC: Citrate carrier; ACC: Acetyl-CoA carboxylase; FAS: Fatty acid synthase.