Nutritional modulation of nonalcoholic fatty liver disease and insulin resistance: human data.
OBJECTIVE
Concomitant with the obesity epidemic, a fatty liver due to nonalcoholic causes has become the most common liver disorder. Nonalcoholic fatty liver disease (NAFLD) covers a range from benign steatosis to nonalcoholic steatohepatitis (NASH), which in turn may progress to cirrhosis. NAFLD predicts, independent of obesity, the metabolic syndrome and type 2 diabetes and can progress to cirrhosis. This review focuses on studies in humans addressing effects of dietary changes in NAFLD.


RESULTS
Cross-sectionally, increased intake of fructose and simple sugars characterizes patients with NAFLD compared with weight-matched controls. Increased fructose intake is also associated with hepatic insulin resistance and fibrosis severity in NASH. Intake of saturated fat may also be increased in NAFLD. Dietary intervention studies have shown that liver volume and fat content changes significantly within a few days in response to caloric restriction or excess despite no or small changes in body weight. Weight loss by bariatric surgery decreases liver fat and inflammation but effects on fibrosis are uncertain. Hepatic insulin sensitivity generally changes in parallel with changes in liver fat content in NAFLD. Human data are limited regarding effects of isocaloric changes in diet composition on liver fat content.


CONCLUSIONS
Maintenance of normal body weight and avoidance of intake of excess lipogenic simple sugars would seem beneficial for prevention of NAFLD and its metabolic consequences.
Yki-Järvinen
Hannele
H
Department of Medicine, University of Helsinki, Helsinki, Finland. ykijarvi@cc.helsinki.fi
D050218:Body Fat Distribution; D001835:Body Weight; D004041:Dietary Fats / Q000008:administration & dosage; D019422:Dietary Sucrose / Q000008:administration & dosage / Q000009:adverse effects*; D002149:Energy Intake; D005234:Fatty Liver / Q000209:etiology / Q000517:prevention & control*; D006801:Humans; D007249:Inflammation / Q000209:etiology; D007333:Insulin Resistance / Q000502:physiology*; D050155:Lipogenesis / Q000502:physiology*; D008099:Liver / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D008103:Liver Cirrhosis / Q000209:etiology
D004041:Dietary Fats; D019422:Dietary Sucrose