Journal
DIABETES OBESITY & METABOLISM
Volume 10, Issue -, Pages 32-42Publisher
WILEY
DOI: 10.1111/j.1463-1326.2008.00969.x
Keywords
beta-cell dysfunction; beta-cell mass; insulin content; insulin secretion; morphometry; pancreatic islet; pathophysiology; type 2 diabetes
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Funding
- Direction de la Recherche Scientifique de la Communaute Francaise de Belgique [ARC 05/10-328]
- Funds National de la Recherche Scientifique Medicale, Bruxelles
- [3.4615.05]
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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 P-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 ill 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 ill the absence of beta-cell dysfunction,
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