Glycated albumin is correlated to insulin resistance and β-cell secretory function in subjects at risk for developing diabetes

Abstract

Insulin resistance and β-cell secretory function represent two main issues in the pathogenesis of type 2 diabetes mellitus (T2DM). Conflicting results have been obtained about the association between glycated albumin (GA) and body mass index (BMI), insulin resistance and β-cell function in diabetic patients. Actually, the relationship (if any) between GA and the markers of glucose homeostasis and insulin resistance in subjects at risk of developing diabetes, has not been completely elucidated yet. Two hundred and one patients undergoing to oral glucose tolerance test (OGTT) were enrolled in the study. Routine laboratory tests, including fasting insulin, were performed at enrollment. GA was measured on plasma-EDTA by quantILab® Glycated Albumin (Instrumentation Laboratory, A Werfen Company) on ILab Taurus analyzer. According to the plasma glucose concentration measured after 2 hours of glucose intake (2h- PG), 13 subjects (6.4%) were classified as impaired glucose tolerance (IGT). GA weakly correlated with fasting plasma glucose (FPG) (r=0.21; P=0.002), with HbA1c (r=0.16; P=0.024) but not with 2h-PG (P=0.7). GA, but not HbA1c, was negatively correlated to HOmeostasis Model Assessment for β cell fuction (HOMA-β) (r2=0.23; P<0.001), to HOMA for insulin resistence (HOMA-IR) (r2=0.15; P<0.0001) and to BMI (r2=0.05; P=0.001). In a stepwise multivariate regression analysis including HbA1c, HOMA-β, plasma albumin, BMI, eGFR, age, FPG, and HOMA-IR as predictors of GA, only HbA1c (β-coefficient: 0.04; P=0.038) and HOMA-β (β-coefficient: -0.01; P<0.0001) were able to predict GA levels (r2=0.26; P<0.001 for the model). Our results demonstrated that GA was associated to HOMA-β and, to a lesser extent, to HOMA-IR and BMI. The increase of GA values can be explained by the reduction of β-cell secretory function in subjects with no significant increase of FPG and 2h-PG.