Too much of a good thing : why it is bad to stimulate the beta cell to secrete insulin

Too much of a good thing : why it is bad to stimulate the beta cell to secrete insulin

Aston-Mourney, K., Proietto, J., Morahan, G. and Andrikopoulos, S. 2008, Too much of a good thing : why it is bad to stimulate the beta cell to secrete insulin, Diabetologia, vol. 51, no. 4, pp. 540-545.

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Title	Too much of a good thing : why it is bad to stimulate the beta cell to secrete insulin
Author(s)	Aston-Mourney, K. Proietto, J. Morahan, G. Andrikopoulos, S.
Journal name	Diabetologia
Volume number	51
Issue number	4
Start page	540
End page	545
Total pages	6
Publisher	Springer
Place of publication	Heidelberg, Germany
Publication date	2008
ISSN	0012-186X 1432-0428
Keyword(s)	C57BL/6 DBA/2 endoplasmic reticulum stress hypersecretion hyperinsulinaemia insulin Islet dysfunction oxidative stress
Summary	In many countries, first- or second-line pharmacological treatment of patients with type 2 diabetes consists of sulfonylureas (such as glibenclamide [known as glyburide in the USA and Canada]), which stimulate the beta cell to secrete insulin. However, emerging evidence suggests that forcing the beta cell to secrete insulin at a time when it is struggling to cope with the demands of obesity and insulin resistance may accelerate its demise. Studies on families with persistent hyperinsulinaemic hypoglycaemia of infancy (PHHI), the primary defect of which is hypersecretion of insulin, have shown that overt diabetes can develop later in life despite normal insulin sensitivity. In addition, in vitro experiments have suggested that reducing insulin secretion from islets isolated from patients with diabetes can restore insulin pulsatility and improve function. This article will explore the hypothesis that forcing the beta cell to hypersecrete insulin may be counterproductive and lead to dysfunction and death via mechanisms that may involve the endoplasmic reticulum and oxidative stress. We suggest that, in diabetes, therapeutic approaches should be targeted towards relieving the demand on the beta cell to secrete insulin.
Language	eng
Field of Research	119999 Medical and Health Sciences not elsewhere classified
Socio Economic Objective	970111 Expanding Knowledge in the Medical and Health Sciences
HERDC Research category	C1.1 Refereed article in a scholarly journal
Copyright notice	©2008, Springer-Verlag
Persistent URL	http://hdl.handle.net/10536/DRO/DU:30047464

Document type:	Journal Article
Collection:	School of Medicine

Citation counts:	Cited 25 times in TR Web of Science
Access Statistics:	10 Abstract Views, 1 File Downloads - Detailed Statistics
Created:	Thu, 30 Aug 2012, 09:32:31 EST

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