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In this issue Daporinad price of the Journal, Yamada et al. explore the impact of ultrasound-diagnosed fatty liver on the incidence of IFG or T2D in Japanese people undergoing a health checkup.11 A total of 12 375 individuals (6799 men and 5576 women) without hyperglycemia or T2D at baseline were re-assessed after 5 years. IFG and T2D were newly diagnosed in 7.6% and 1% of men, and 3.8% and 0.5% of women, respectively, within the study period. In both sexes, the prevalence of newly diagnosed IFG and T2D was significantly higher in the participants with fatty liver than among those without fatty liver, and after adjustment for the other risk factors, fatty liver remained an independent risk factor for IFG and/or T2D. The impact of fatty liver on incidence of IFG and T2D was stronger among participants with a lower BMI. Therefore, the presence of fatty liver may be a better predictor for development of T2D than obesity

itself, and it can be considered to be an early predictor of T2D. In general, this is a well written and concise manuscript with a clear message, and answers a question that is important and significant in public health. Furthermore, it has the strength of studying click here a large number of individuals. Some limitations of this study include the lack of liver enzymes and OGTT at baseline, the use of a single result of fasting plasma glucose (FPG) for diagnosis of diabetes at follow up, and lack of rigorous exclusion of other etiologies of fatty liver, making it difficult to draw conclusions regarding second the metabolic risk among subjects with NAFLD. It should be noted that regional guidelines recommend an OGTT be performed at diagnosis of NAFLD when FPG is more than 5.6 mmol/L12, and several studies now report a much higher prevalence of glucose intolerance and established T2D at diagnosis of NAFLD when OGTT is routinely performed.14–16 Both T2D

and hepatogenous diabetes (complicating cirrhosis) are associated with increased liver-related morbidity and mortality in cirrhotic patients regardless of etiology.1 Unlike the hepatogenous diabetes attributed to cirrhosis, T2D in NAFLD is more frequently associated with risk factors such as age, BMI and family history of T2D.1,4–11 It constitutes a risk factor for NASH, for fibrotic progression to cirrhosis and ultimately hepatocellular carcinoma. The finding of diabetes is thus associated with an increased risk of all-cause death and liver-related mortality in patients with NAFLD, and diabetic and cardiovascular risk may compete with liver-related complications in dictating the final outcome.1,3 The biological mechanisms by which NAFLD contributes to a higher risk of developing T2D are not fully understood. However, the fatty liver could contribute in the same way as visceral adipose tissue to insulin resistance, systemic inflammation and oxidative stress, while decreased serum adiponectin concentrations might also be part of the mechanism.