Improved β-cell function rather than increased insulin sensitivity is associated with reduction in hemoglobin A1c in newly diagnosed Type 2 diabetic patients treated with metformin
2014
β-cell
dysfunction and decreased insulin sensitivity are believed to be two chief
mechanisms that participate in deterioration of glycemic control in Type 2
diabetes. Meformin is widely accepted as the first-line oral agent in the treatment
of Type 2 diabetes. However, the relative contributions of improved β-cell function and increased insulin
sensitivity to reduction in hemoglobin A1c (HbA1c) are unclear in newly diagnosed
Type 2 diabetic patients treated with metformin. We investigated β-cell function and insulin sensitivity
in relation to reduction in HbA1c in 20 newly diagnosed Type 2 diabetic
patients (17 men and 3 women, mean age 49.1 ± 10.1 years, mean body mass index
26.4 ± 5.2 kg/m2) treated with metformin for 16 weeks. We used
homeostasis model assessment (HOMA) 2%B and HOMA2%S as estimates of β-cell function and insulin sensitivity,
respectively. Median HOMA2%B and HOMA2%S significantly increased from 38.8 to
68.8 (p p = 0.004),
respectively. In univariate regression analysis, reduction in HbA1c was highly
correlated with change in HOMA2%B (r = -0.866, p r = -0.264, p = 0.260). Furthermore,
multivariate regression analysis with reduction in HbA1c as a dependent
variable showed that increase in HOMA2%B but not that in HOMA2%S was a
significant dependent variable (β = -0.847, p β-cell function rather than increased
insulin sensitivity is associated with reduction in HbA1c. These results
suggest that metformin reduces HbA1c chiefly through improved β-cell function rather than increased insulin
sensitivity in patients with newly diagnosed Type 2 diabetes.
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