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Pathogenetic Considerations of Idiopathic Diabetes

  • Bruno W. Volk
  • Klaus F. Wellmann

Abstract

The hypothesis that idiopathic diabetes is a result of insufficient secretion of insulin seemed to be confirmed by many earlier experimental studies carried out around the turn of the century. This viewpoint was based on the studies of Von Mering and Minkowski1 who, in 1889, were the first to observe that removal of the pancreas causes diabetes in the dog. The discovery of insulin by Banting and Best2 in 1922 seemed to support this hypothesis, since the administration of pancreatic extracts could correct the metabolic abnormalities in diabetes. This was in keeping with the frequently observed atrophy of the pancreatic islets,3–7 the decrease of extractable insulin8–10 in pancreases of juvenile diabetics, and the occurrence of interacinar fibrosis, insular fibrosis, and hyalinization in the pancreases of maturity-onset diabetics.11 Moreover, quantitative studies by various authors indicated a relative increase of A cells in many diabetic pancreases associated with a concomitant decrease of the B cells.7,12–14

Keywords

Diabetic Individual Glucagon Level Pancreatic Glucagon Juvenile Diabetic Blood Sugar Concentration 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Plenum Press, New York 1977

Authors and Affiliations

  • Bruno W. Volk
    • 1
  • Klaus F. Wellmann
    • 1
  1. 1.Isaac Albert Research Institute of the Kingsbrook Jewish Medical Center, and Downstate Medical CenterState University of New YorkBrooklynUSA

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