Significantly Decreased Islet β Cell Function is Closely Associated with Hyperglycemia in Chronic Hepatitis B Patients

Abstract

Aim. This study is aimed at the characteristics of glucose metabolism and islet β cell function evaluated by the homeostasis model assessment of β cell function (HOMA-β) value and its risk factors in chronic hepatitis B (CHB) patients. Method. This cross-sectional study recruited 110 CHB patients (CHB group) and 110 patients without hepatitis B virus (non-HBV group); the groups were matched according to sex, age, and body mass index under the same glucose metabolism status. The risk factors, characteristics, and differences in glucose metabolism and HOMA-β values between the two groups were analyzed. Results. The abnormal glucose metabolism rate was higher in CHB patients with liver cirrhosis (LC) or hepatitis B envelope antigen (HBeAg) (−) status. In addition, under the same glucose metabolism status, the fasting plasma glucose (FPG) levels and 2-hour postprandial plasma glucose (2h-PG) levels in the CHB group were higher, while the HOMA-β values were significantly lower and the homeostasis model assessment of insulin resistance (HOMA-IR) value was not higher than that in the non-HBV group (all $P<0.0001$ ). Further analyses revealed that the main risk factors for abnormal glucose metabolism were HBeAg (−) status and hepatitis B envelope antibody levels. But HBV serological and virological indicators had no effects on the HOMA-β values. Conclusion. Islet β cell function in patients with CHB was compromised, which is closely associated with fasting and postprandial hyperglycemia in chronic hepatitis B patients. Further research should be done to verify the compromised islet β cell function and then to investigate the mechanisms behind the effect of hepatitis B virus infection on islet β cell function in CHB patients.