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Insulin resistance as a programmed response to fetal undernutrition

Insulin resistance as a programmed response to fetal undernutrition Diabetologia (1996) 39:1119-1122 Diabetologia 9 Springer-Verlag1996 For debates D.I.W. Phillips Metabolic Programming Group, MRC Environmental Epidemiology Unit, (University of Southampton), Southampton General Hospital, Southampton, UK Impaired tissue sensitivity to the action of insulin (insulin resistance) is a major abnormality underlying non-insulin-dependent diabetes mellitus (NIDDM). Insulin resistance is also associated with hypertension and dyslipidaemia, and may be an important and preventable cause of heart disease [1]. Although influenced by ageing, obesity, physical inactivity and certain drugs, current opinion holds that insulin resistance is hereditary in origin. Recent evidence, however, suggests a new hypothesis - that insulin resistance may occur as a consequence of the persistence of a fetal response to undernutrition. It is suggested that the undernourished fetus makes metabolic adaptations from which it benefits in the short term by increasing fuel availability but that these adaptations become permanently programmed and persist throughout life. Fetal growth and N I D D M between low birthweight and NIDDM is due to babies who were small for their gestational age rather than premature [3]. Although obesity later in life adds to the effects of infancy, the association with birthweight is independent of the level or distribution of adult obesity. Where more http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Diabetologia Springer Journals

Insulin resistance as a programmed response to fetal undernutrition

Phillips, D.
Diabetologia , Volume 39 (9) – Sep 1, 1996
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References (40)

Publisher
Springer Journals
Copyright
Copyright © 1996 by Springer-Verlag
Subject
Medicine & Public Health; Human Physiology; Internal Medicine; Metabolic Diseases
ISSN
0012-186X
eISSN
1432-0428
DOI
10.1007/BF00400663
Publisher site
See Article on Publisher Site

Abstract

Diabetologia (1996) 39:1119-1122 Diabetologia 9 Springer-Verlag1996 For debates D.I.W. Phillips Metabolic Programming Group, MRC Environmental Epidemiology Unit, (University of Southampton), Southampton General Hospital, Southampton, UK Impaired tissue sensitivity to the action of insulin (insulin resistance) is a major abnormality underlying non-insulin-dependent diabetes mellitus (NIDDM). Insulin resistance is also associated with hypertension and dyslipidaemia, and may be an important and preventable cause of heart disease [1]. Although influenced by ageing, obesity, physical inactivity and certain drugs, current opinion holds that insulin resistance is hereditary in origin. Recent evidence, however, suggests a new hypothesis - that insulin resistance may occur as a consequence of the persistence of a fetal response to undernutrition. It is suggested that the undernourished fetus makes metabolic adaptations from which it benefits in the short term by increasing fuel availability but that these adaptations become permanently programmed and persist throughout life. Fetal growth and N I D D M between low birthweight and NIDDM is due to babies who were small for their gestational age rather than premature [3]. Although obesity later in life adds to the effects of infancy, the association with birthweight is independent of the level or distribution of adult obesity. Where more

Journal

Diabetologia – Springer Journals

Published: Sep 1, 1996

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