Fetal growth and insulin secretion in adult life |
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Authors: | Dr D I W Phillips S Hirst P M S Clark C N Hales C Osmond |
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Institution: | (1) Metabolic Programming Group, University of Southampton, Southampton General Hospital, Tremona Road, SO9 4XY Southampton, UK;(2) Department of Clinical Biochemistry, University of Cambridge, Addenbrooke's Hospital, Cambridge, UK;(3) MRC Environmental Epidemiology Unit, University of Southampton, Southampton General Hospital, Southampton, UK |
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Abstract: | Summary Recent studies suggest that NIDDM is linked with reduced fetal and infant growth. Observations on malnourished infants and studies of experimental animals exposed to protein energy or protein deficiency in fetal or early neonatal life suggest that the basis of this link could lie in the detrimental effects of poor early nutrition on the development of the beta cells of the islets of Langerhans. To test this hypothesis we have measured insulin secretion following an IVGTT in a sample of 82 normoglycaemic and 23 glucose intolerant subjects who were born in Preston, England, and whose birthweight and body size had been recorded at birth. The subjects with impaired glucose tolerance had lower first phase insulin secretion than the normoglycaemic subjects (mean plasma insulin concentrations 3 min after intravenous glucose 416 vs 564 pmol/l, p=0.04). Insulin secretion was higher in men than women (601 vs 457 pmol/l, P=0.02) and correlated with fasting insulin level (p=0.04). However, there was no relationship between insulin secretion and the measurements of prenatal growth in either the normoglycaemic or glucose intolerant subjects. These results argue against a major role for defective insulin secretion as a cause of glucose intolerance in adults who were growth retarded in pre-natal life.Abbreviations NIDDM
Non-insulin-dependent diabetes
- OGTT
oral glucose tolerance test
- IVGTT
intravenous glucose tolerance test |
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Keywords: | NIDDM insulin secretion fetal growth programming |
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