The Role of Markers of Low-Grade Inflammation for the Early Time Course of Glycemic Control, Glucose Disappearance Rate, and β-Cell Function in Recently Diagnosed Type 1 and Type 2 Diabetes.

Abstract

Inflammatory processes are involved in the progression of insulin resistance and β-cell dysfunction in individuals with prediabetes and contribute to the development of diabetes. We hypothesized that higher levels of biomarkers of low-grade inflammation are associated with the early progression of recently diagnosed diabetes. Within the prospective German Diabetes Study, patients with recently diagnosed type 1 (n = 42) and type 2 (n = 94) diabetes underwent detailed metabolic characterization within the first year after diagnosis and 2 years thereafter. Associations between changes in markers of low-grade inflammation with changes in glycemic control, β-cell function, and glucose disappearance rate were assessed using multivariable linear regression analysis. Associations were adjusted for age, sex, BMI, smoking status, and 2-year changes in BMI, smoking status, and glucose-lowering medication. Patients with type 1 and type 2 diabetes exhibited good glucometabolic control at baseline (mean HbA1c 7.08 ± 1.58% [54 ± 17 mmol/mol] and 6.43 ± 0.98% [47 ± 11 mmol/mol], respectively) and 2 years thereafter (mean HbA1c 7.03 ± 1.20% [53 ± 13 mmol/mol] and 6.62 ± 1.14% [49 ± 13], respectively). Two-year increases of high-sensitivity C-reactive protein, soluble E-selectin (sE-selectin), and soluble intercellular adhesion molecule-1 in type 2 diabetes and of IL-18 in type 1 diabetes were associated with 2-year increases of HbA1c. Additionally, 2-year increases of sE-selectin were associated with 2-year decreases of prehepatic β-cell function in type 2 diabetes (all P < 0.05). These data indicate that with the clinical onset of diabetes, low-grade inflammation relates to worsening of glycemia and that endothelial activation may contribute to decreasing β-cell function.