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International Journal of Experimental Diabetes Research
Volume 3, Issue 3, Pages 153-158

Type 2 Diabetes—Effect of Compensatory Oversecretion as a Reason for β-Cell Collapse

1Department of Internal Medicine, Medical Faculty, Norwegian University of Science and Technology, Trondheim, Norway
2Department of Molecular Medicine, Karolinska Institute, Stockholm, Sweden
3Department of Medicine, University Hospital of Trondheim, Trondheim 7006, Norway

Copyright © 2002 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Insulin secretion declines progressively before and during the course of type 2 diabetes. Evidence indicates that this process is, in part, secondary to increased requirement for insulin secretion that is brought about by insulin resistance and by hyperglycemia. The effects of over-secretion extend far beyond a mere reduction of available insulin stores and may cause not only functional but also structural damage. The time is ripe for clinical studies, which explore the therapeutic potential of reducing over-secretion.