Send to

Choose Destination
J Diabetes Investig. 2011 Nov 30;2(6):483-9. doi: 10.1111/j.2040-1124.2011.00134.x.

Impact of glucose tolerance on the severity of non-alcoholic steatohepatitis.

Author information

Departments of Endocrinology and Metabolism.
Gastroenterology, Graduate School of Medicine, Yokohama City University, Yokohama, Japan.


Aims/Introduction:  We investigated the relationship between non-alcoholic steatohepatitis (NASH) and different stages of fasting plasma glucose (FPG) concentrations, and the association between factors related to glucose tolerance and severity of NASH.


  A total of 147 patients with non-alcoholic fatty liver disease (NAFLD) who had undergone a liver biopsy were divided into three groups: a normal glucose tolerance (NGT) group, an impaired fasting glucose (IFG) group and a diabetes (DM) group. In addition, to investigate progression factors of NASH in the DM group, we divided the diabetic patients into two groups: a group with NASH (NASH group) and a group without NASH, the simple steatosis (SS) group. The relationship between the patients' clinical parameters and the severity of NAFLD/NASH were analyzed.


  In the patients with liver biopsies, the IFG group had the highest percentage of NASH. There was no correlation between FPG and either total NAFLD activity scores (NAS) or staging of NASH, but the fasting serum insulin was correlated significantly with both, even after adjusting for age, sex and body mass index. Among the diabetic patients, the fasting insulin values in the NASH group were significantly higher than in the SS group, but there were no differences in FPG or A1c values between the two groups. The fasting serum insulin correlated significantly with total NAS, but the FPG and A1c values did not.


  A high percentage of the IFG group developed NASH. Hyperinsulinemia, but not hyperglycemia, was associated with severity of NASH. (J Diabetes Invest, doi: 10.1111/j.2040-1124.2011.00134.x, 2011).


Hyperglycemia; Hyperinsulinemia; Non‐alcoholic steatohepatitis

Supplemental Content

Full text links

Icon for Wiley Icon for PubMed Central
Loading ...
Support Center