Objective: In 2003, the American Diabetes Association recommended that the lower limit for the diagnosis of impaired fasting glucose (IFG) should be reduced from 110 to 100 mg/dL in the analysis of the associated risk factors of IFG. It has been proposed that liver dysfunction may contribute to the development of type 2 diabetes. A primary aim was to investigate the relationship between liver enzyme and insulin resistance (IR) in IFG group. The secondary aim was to investigate IR and beta-cell function assessed by homeostasis model assessment (HOMA-IR and HOMA-%B, respectively) in subjects with fasting plasma glucose (FPG) between 100 and 109 mg/dL.
Methods: We enrolled 284 subjects whose medical history and physical examination required tests to screen for metabolic abnormalities. In addition, we also excluded all factors affecting glucose or insulin metabolism. According to the FPG level, they were divided into the following groups: group A, FPG < 100 mg/dL; group B, FPG = 100 to 109 mg/dL; group C, FPG = 110 to 125 mg/dL.
Results: Group B as compared with group A had significant increase of HOMA-IR and decrease of HOMA-%B. Among the whole population, the fasting insulin level, the fasting glucose, HbA1c, HOMA-IR, alanine aminotransferase, gamma-glutamyltranspeptidase, aspartate aminotransferase, and the diastolic blood pressure all increased significantly as the glycemic status progressed, whereas HOMA-%B levels decreased significantly as the glycemic status progressed. The lipid profile, alkaline phosphatase, and systolic blood pressure did not differ significantly among 3 different glycemic classifications.
Conclusions: Study results indicate that, first, there was a significant decrease of insulin sensitivity and insulin secretion in subjects with fasting glucose from 100 to 109 mg/dL compared with subjects with normal fasting glucose. Second, alanine aminotransferase, aspartate aminotransferase, and gamma-glutamyltranspeptidase were associated with IR as the glycemic status progressed in the IFG group.