For a long time, fatty liver or hepatic steatosis was considered as a benign manifestation. However, recent data indicate a wide spectrum of clinical and pathological manifestations that subjects with nonalcoholic hepatic steatosis develop, which are termed as nonalcoholic fatty liver disease (NAFLD). Interestingly, the manifestations of NAFLD are similar to those seen in patients with alcoholic liver disease and range from mild hepatic steatosis, steatohepatitis, fibrosis, to cirrhosis (1–3), and, rarely, to hepatocellular carcinoma (4–6).

Nonalcoholic hepatic steatosis is usually found in obese subjects (1–3, 7). Recent studies have documented a strong relationship between hepatic steatosis and insulin resistance (1, 8–13), which may account for hepatic steatosis in nonobese and even lean subjects (11–14). The prevalence of other metabolic abnormalities associated with insulin resistance such as abnormal glucose tolerance, hypertriglyceridemia, and low levels of high-density lipoprotein cholesterol is also high in subjects with NAFLD (2, 9, 10). The underlying mechanisms for the association of insulin resistance and obesity to hepatic steatosis remain unclear. To explain these relationships, it has been hypothesized that excess of “portal” or intraperitoneal fat can increase flux of free fatty acids via portal vein directly to the liver and, thus, may induce hepatic insulin resistance and hepatic steatosis (15). In contrast, we previously reported that hepatic insulin resistance in men was more strongly related to sc abdominal fat mass than to intraperitoneal fat mass (16, 17). The possibilities that intraperitoneal fat mass may preferentially affect hepatic very low-density lipoprotein-triglyceride secretion and hepatic fat accumulation still remain. Thus, the relationships between regional adiposity, insulin resistance, and hepatic steatosis continue to be an area of active investigation.