Abstract

Objective— Glucose fluctuations trigger activation of oxidative stress, a main mechanism leading to secondary diabetes complications. We evaluated the relationship between glycemic variability and ß-cell dysfunction.

Research design and methods— We conducted a cross-sectional study in 59 patients with type 2 diabetes (age 64.2 ± 8.6 yrs, HbA1c 6.5 ± 1.0 %, BMI 29.8 ± 3.8 kg/m²; mean ± SD) using either oral hypoglycemic agents (OHA, n = 34) or diet alone (non-users). As measure of glycemic variability, the mean amplitude of glycemic excursions (MAGE) was computed from continuous glucose monitoring data recorded over three consecutive days. The relationships between MAGE, ß-cell function, and clinical parameters were assessed by including postprandial (PBCF) and basal ß-cell function (BBCF).obtained by a model-based method from plasma C-peptide and plasma glucose during a mixed-meal test as well as insulin sensitivity (HOMA2-%S), clinical factors, carbohydrate intake, and type of OHA.

Results— MAGE was non-linearly correlated with PBCF (r = 0.54, P < 0.001) and with BBCF (r = 0.31, P = 0.025) in OHA users but failed to correlate with these parameters in non-users (PBCF; P = 0.21 and BBCF; P = 0.07). The stepwise multiple regression analysis demonstrated that PBCF and OHA-combination treatment were independent contributors to MAGE (R² = 0.50, P < 0.010) whereas insulin sensitivity, carbohydrate intake, and non-glycemic parameters failed to contribute..

Conclusions— The postprandial ß-cell function appears to be an important target to reduce glucose fluctuations in OHA-treated type 2 diabetes.