Parallel dysfunctions of pancreatic A, B and PP cells in insulin dependent diabetes.
To test the possibility that insulitis might play an etiological role in the pathogenesis of insulin dependent diabetes, functions of 3 kinds of islet constituting cells (A, B and PP cells) were estimated by quantifying secretory responses of glucagon-, C-peptide-and pancreatic polypeptide-producing cells to hyperglycemia and hypoglycemia. In insulin dependent diabetes, all 3 hormonal responses were severely impaired to the same extent. On the other hand, 3 islet cell functions were uniformly but less severely impaired in insulin independent diabetics without a diabetic family history. These results suggest that A, B, and PP cells of islet of Langerhans are evenly destroyed in parallel fashion at least in insulin dependent diabetes and in some insulin independent diabetes, suggesting insulitis as a possible cause of these types of diabetes.
D001786:Blood Glucose / Q000378:metabolism; D002096:C-Peptide / Q000097:blood; D003920:Diabetes Mellitus / Q000503:physiopathology*; D005934:Glucagon / Q000097:blood; D005947:Glucose / Q000494:pharmacology; D006801:Humans; D007328:Insulin / Q000494:pharmacology; D007515:Islets of Langerhans / Q000503:physiopathology*; D010191:Pancreatic Polypeptide / Q000097:blood
D001786:Blood Glucose; D002096:C-Peptide; D007328:Insulin; D010191:Pancreatic Polypeptide; D005934:Glucagon; D005947:Glucose