The accelerator hypothesis: weight gain as the missing link between Type I and Type II diabetes View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2001-07

AUTHORS

T. J. Wilkin

ABSTRACT

Blood glucose concentrations are controlled by a loop incorporating two components, the beta cells which secrete insulin and the insulin-sensitive tissues (liver, muscle, adipose) which respond to it. Loss of blood glucose control might result from failure of the beta cells to secrete insulin, resistance of the tissues to its action, or a combination of both. The distinctions between Type I (insulin-dependent) and Type II (non-insulin-dependent) diabetes mellitus are becoming increasingly blurred both clinically and aetiologically, where beta-cell insufficiency is the shared characteristic. The 'Accelerator Hypothesis' identifies three processes which variably accelerate the loss of beta cells through apoptosis: constitution, insulin resistance and autoimmunity. None of the accelerators leads to diabetes without excess weight gain, a trend which the 'Accelerator Hypothesis' deems central to the rising incidence of both types of diabetes in the industrially developed world. Weight gain causes an increase in insulin resistance, which results in the weakening of glucose control. The rising blood glucose (glucotoxicity) accelerates beta-cell apoptosis directly in all and, by inducing beta-cell immunogens, further accelerates it in a subset genetically predisposed to autoimmunity. Rather than overlap between two types of diabetes, the 'Accelerator Hypothesis' envisages overlay. Body mass is central to the development and rising incidence of all diabetes. Only tempo distinguishes the 'types'. The control of weight gain, and with it insulin resistance, could be the means of minimising both. More... »

PAGES

914-922

References to SciGraph publications

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s001250100548

DOI

http://dx.doi.org/10.1007/s001250100548

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1048570619

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/11508279


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