The thrifty phenotype hypothesis
The thrifty phenotype hypothesis
The thrifty phenotype hypothesis proposes that the epidemiological associations between poor fetal and infant growth and the subsequent development of type 2 diabetes and the metabolic syndrome result from the effects of poor nutrition in early life, which produces permanent changes in glucose-insulin metabolism. These changes include reduced capacity for insulin secretion and insulin resistance which, combined with effects of obesity, ageing and physical inactivity, are the most important factors in determining type 2 diabetes.
Since the hypothesis was proposed, many studies world-wide have confirmed the initial epidemiological evidence, although the strength of the relationships has varied from one study to another. The relationship with insulin resistance is clear at all ages studied. Less clear is the relationship with insulin secretion. The relative contribution of genes and environment to these relationships remains a matter of debate. The contributions of maternal hyperglycaemia and the trajectory of postnatal growth need to be clarified.
5-20
Hales, C. Nicholas
090ef264-50ee-4c98-b06a-7cba79b95286
Barker, David J.P.
5c773838-b094-4ac1-999b-b5869717f243
2001
Hales, C. Nicholas
090ef264-50ee-4c98-b06a-7cba79b95286
Barker, David J.P.
5c773838-b094-4ac1-999b-b5869717f243
Hales, C. Nicholas and Barker, David J.P.
(2001)
The thrifty phenotype hypothesis.
British Medical Bulletin, 60 (1), .
Abstract
The thrifty phenotype hypothesis proposes that the epidemiological associations between poor fetal and infant growth and the subsequent development of type 2 diabetes and the metabolic syndrome result from the effects of poor nutrition in early life, which produces permanent changes in glucose-insulin metabolism. These changes include reduced capacity for insulin secretion and insulin resistance which, combined with effects of obesity, ageing and physical inactivity, are the most important factors in determining type 2 diabetes.
Since the hypothesis was proposed, many studies world-wide have confirmed the initial epidemiological evidence, although the strength of the relationships has varied from one study to another. The relationship with insulin resistance is clear at all ages studied. Less clear is the relationship with insulin secretion. The relative contribution of genes and environment to these relationships remains a matter of debate. The contributions of maternal hyperglycaemia and the trajectory of postnatal growth need to be clarified.
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Published date: 2001
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Local EPrints ID: 25576
URI: http://eprints.soton.ac.uk/id/eprint/25576
ISSN: 0007-1420
PURE UUID: 183012ec-38f7-4c5b-923a-d956c8a98af3
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Date deposited: 20 Apr 2006
Last modified: 22 Jul 2022 20:31
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Author:
C. Nicholas Hales
Author:
David J.P. Barker
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