Cellular composition of the human diabetic pancreas

J Rahier, RM Goebbels, JC Henquin - Diabetologia, 1983 - Springer
J Rahier, RM Goebbels, JC Henquin
Diabetologia, 1983Springer
Insulin, glucagon, somatostatin and pancreatic polypeptide cells were stained by
immunoperoxidase techniques and quantitated morphometrically in sections of pancreases
obtained from eight control subjects, four Type 1 (insulin-dependent) and eight Type 2 (non-
insulin-dependent) diabetic patients. The whole pancreas was studied to take into
consideration the heterogeneous distribution of the different cell types. From the volume
density of each cell type, and the weight of each lobe of the pancreas, the total mass of …
Summary
Insulin, glucagon, somatostatin and pancreatic polypeptide cells were stained by immunoperoxidase techniques and quantitated morphometrically in sections of pancreases obtained from eight control subjects, four Type 1 (insulin-dependent) and eight Type 2 (non-insulin-dependent) diabetic patients. The whole pancreas was studied to take into consideration the heterogeneous distribution of the different cell types. From the volume density of each cell type, and the weight of each lobe of the pancreas, the total mass of endocrine tissue was calculated. It averaged 1395 mg in control subjects, 413 mg in Type 1 and 1449 mg in Type 2 diabetic patients. The loss of endocrine tissue observed in the Type 1 patients was almost restricted to the lobe poor in pancreatic polypeptide cells. In these patients, B cells were practically absent (at the most seven per section), but the ‘atrophic islets’ still contained numerous A, D, or pancreatic polypeptide cells. The mass of A, D and pancreatic polypeptide cells and the ratio of D to A cells were not different from those measured in the control subjects. This shows that the disappearance of B cells in Type 1 diabetes has no preferential effect on any other endocrine cell of the pancreas. In Type 2 diabetes, the mass of A cells was increased, whereas that of B, D and pancreatic polypeptide cells was not changed. This hyperplasia of A cells leads to a decrease in the ratio of B to A and of D to A cells. These alterations may enlighten certain aspects of the physiopathology of Type 2 diabetes.
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