Insulin resistance in Nonalcoholic fatty liver disease (NAFLD) is characterized by diminutions in whole-body, hepatic, and adipose tissue insulin sensitivity NAFLD. NAFLD is a common liver disorder which is strappingly connected with insulin resistance and type 2 diabetes. This condition will only increase in occurrence, with the increase in the number of individuals who are overweight or obese. The mechanisms underlying the growth of NAFLD are not wholly understood, but probably involve a combination of increased free fatty acids (FFA). And possibly decreased lipid oxidation in the liver as a result of insulin resistance.

The mechanisms underlying the gathering of fat in the liver may include excess dietary fat, increased delivery of free fatty acids to the liver, insufficient fatty acid oxidation, and increased de novo lipogenesis. Insulin resistance may improve hepatic fat accumulation by increasing free fatty acid delivery and by the effect of hyperinsulinemia to stimulate anabolic processes. The influence of weight loss, metformin, and thiazolidinediones, all treatments aimed at refining insulin sensitivity, as well as other agents such as vitamin E, have been assessed in patients with NAFLD and have shown some advantage.

Insulin resistance is a foremost feature of NAFLD that, in some patients, can progress to steatohepatitis. Insulin resistance may be an essential defect in NAFLD that reduced insulin receptiveness at the level of the adipocyte may contribute to hepatic steatosis by excess FFA flux to the liver. Forthcoming research must focus on illuminating the relationship between hepatic and peripheral insulin resistance and the development of hepatic steatosis.

Source: The Journal of Clinical Endocrinology & Metabolism, 91(12), 2006, 4753–4761