Author(s): Rahier J, Guiot Y, Goebbels RM, Sempoux C, Henquin JC, Rahier J, Guiot Y, Goebbels RM, Sempoux C, Henquin JC, Rahier J, Guiot Y, Goebbels RM, Sempoux C, Henquin JC, Rahier J, Guiot Y, Goebbels RM, Sempoux C, Henquin JC
Abstract Share this page
Abstract Decreases in both beta-cell function and number can contribute to insulin deficiency in type 2 diabetes. Here, we quantified the beta-cell mass in pancreas obtained at autopsy of 57 type 2 diabetic (T2D) and 52 non-diabetic subjects of European origin. Sections from the body and tail were immunostained for insulin. The beta-cell mass was calculated from the volume density of beta-cells (measured by point-counting methods) and the weight of the pancreas. The pancreatic insulin concentration was measured in some of the subjects. beta-cell mass increased only slightly with body mass index (BMI). After matching for BMI, the beta-cell mass was 41\% (BMI < 25) and 38\% (BMI 26-40) lower in T2D compared with non-diabetic subjects, and neither gender nor type of treatment influenced these differences. beta-cell mass did not correlate with age at diagnosis but decreased with duration of clinical diabetes (24 and 54\% lower than controls in subjects with <5 and >15 years of overt diabetes respectively). Pancreatic insulin concentration was 30\% lower in patients. In conclusion, the average beta-cell mass is about 39\% lower in T2D subjects compared with matched controls. Its decrease with duration of the disease could be a consequence of diabetes that, with further impairment of insulin secretion, contributes to the progressive deterioration of glucose homeostasis. We do not believe that the small difference in beta-cell mass observed within 5 years of onset could cause diabetes in the absence of beta-cell dysfunction.
This article was published in Diabetes Obes Metab
and referenced in Diabetes Case Reports