Pancreatic β-cell mass in European subjects with type 2 diabetes

• Published in: Diabetes, obesity & metabolism Vol. 10; no. s4; pp. 32 - 42
• Main Authors: Rahier, J, Guiot, Y, Goebbels, R.M, Sempoux, C, Henquin, J.C
• Format: Journal Article
• Language: English
• Published: Oxford, UK Oxford, UK : Blackwell Publishing Ltd 01.11.2008; Blackwell Publishing Ltd
• Subjects: Adult; Aged; Aged, 80 and over; Autopsy - methods; Blood Glucose - metabolism; Body Mass Index; Diabetes Mellitus, Type 2 - pathology; Disease Progression; European Continental Ancestry Group; Female; Humans; insulin content; Insulin Resistance - physiology; insulin secretion; Insulin-Secreting Cells - metabolism; Insulin-Secreting Cells - pathology; Male; Middle Aged; morphometry; noninsulin-dependent diabetes mellitus; Obesity - complications; Pancreas - pathology; pancreatic islet; pathophysiology; type 2 diabetes; β-cell dysfunction; β-cell mass
• ISSN: 1462-8902; 1463-1326; 1463-1326
• DOI: 10.1111/j.1463-1326.2008.00969.x

Decreases in both β-cell function and number can contribute to insulin deficiency in type 2 diabetes. Here, we quantified the β-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 β-cell mass was calculated from the volume density of β-cells (measured by point-counting methods) and the weight of the pancreas. The pancreatic insulin concentration was measured in some of the subjects. β-cell mass increased only slightly with body mass index (BMI). After matching for BMI, the β-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. β-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 β-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 β-cell mass observed within 5 years of onset could cause diabetes in the absence of β-cell dysfunction.