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      Developmental Programming in Response to Maternal Overnutrition

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          Abstract

          Metabolic disorders have seen an increased prevalence in recent years in developed as well as developing countries. While it is clear lifestyle choices and habits have contributed to this epidemic, mounting evidence suggests the nutritional milieu during critical stages of development in early life can “program” individuals to develop the metabolic syndrome later in life. Extensive epidemiological data presents an association between maternal obesity and nutrition during pregnancy and offspring obesity, and a number of animal models have been established in order to uncover the underlying mechanisms contributing to the programming of physiological systems. It is hard to distinguish the causal factors due to the complex nature of the maternal–fetal relationship; however, in order to develop adequate prevention strategies it is vital to identify which maternal factor(s) – be it the diet, diet-induced obesity or weight gain – and at which time during early development instigate the programmed phenotype. Curtailing the onset of obesity at this early stage in life presents a promising avenue through which to stem the growing epidemic of obesity.

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          Most cited references 91

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          Type 2 (non-insulin-dependent) diabetes mellitus, hypertension and hyperlipidaemia (syndrome X): relation to reduced fetal growth

          Two follow-up studies were carried out to determine whether lower birthweight is related to the occurrence of syndrome X-Type 2 (non-insulin-dependent) diabetes mellitus, hypertension and hyperlipidaemia. The first study included 407 men born in Hertfordshire, England between 1920 and 1930 whose weights at birth and at 1 year of age had been recorded by health visitors. The second study included 266 men and women born in Preston, UK, between 1935 and 1943 whose size at birth had been measured in detail. The prevalence of syndrome X fell progressively in both men and women, from those who had the lowest to those who had the highest birthweights. Of 64-year-old men whose birthweights were 2.95 kg (6.5 pounds) or less, 22% had syndrome X. Their risk of developing syndrome X was more than 10 times greater than that of men whose birthweights were more than 4.31 kg (9.5 pounds). The association between syndrome X and low birthweight was independent of duration of gestation and of possible confounding variables including cigarette smoking, alcohol consumption and social class currently or at birth. In addition to low birthweight, subjects with syndrome X had small head circumference and low ponderal index at birth, and low weight and below-average dental eruption at 1 year of age. It is concluded that Type 2 diabetes and hypertension have a common origin in sub-optimal development in utero, and that syndrome X should perhaps be re-named "the small-baby syndrome".
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            Fetal and infant growth and impaired glucose tolerance at age 64.

            To discover whether reduced fetal and infant growth is associated with non-insulin dependent diabetes and impaired glucose tolerance in adult life. Follow up study of men born during 1920-30 whose birth weights and weights at 1 year were known. Hertfordshire, England. 468 men born in east Hertfordshire and still living there. Fasting plasma glucose, insulin, proinsulin, and 32-33 split pro-insulin concentrations and plasma glucose and insulin concentrations 30 and 120 minutes after a 75 g glucose drink. 93 men had impaired glucose tolerance or hitherto undiagnosed diabetes. They had had a lower mean birth weight and a lower weight at 1 year. The proportion of men with impaired glucose tolerance fell progressively from 26% (6/23) among those who had weighted 18 lb (8.16 kg) or less at 1 year to 13% (3/24) among those who had weighed 27 lb (12.25 kg) or more. Corresponding figures for diabetes were 17% (4/23) and nil (0/24). Plasma glucose concentrations at 30 and 120 minutes fell with increasing birth weight and weight at 1 year. Plasma 32-33 split proinsulin concentration fell with increasing weight at 1 year. All these trends were significant and independent of current body mass. Blood pressure was inversely related to birth weight and strongly related to plasma glucose and 32-33 split proinsulin concentrations. Reduced growth in early life is strongly linked with impaired glucose tolerance and non-insulin dependent diabetes. Reduced early growth is also related to a raised plasma concentration of 32-33 split proinsulin, which is interpreted as a sign of beta cell dysfunction. Reduced intrauterine growth is linked with high blood pressure, which may explain the association between hypertension and impaired glucose tolerance.
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              Type 2 (non-insulin-dependent) diabetes mellitus: the thrifty phenotype hypothesis.

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                Author and article information

                Journal
                Front Genet
                Front. Gene.
                Frontiers in Genetics
                Frontiers Research Foundation
                1664-8021
                03 June 2011
                2011
                : 2
                Affiliations
                1Metabolic Research Laboratories, Institute of Metabolic Science, Addenbrooke’s Hospital, University of Cambridge Cambridge, UK
                Author notes

                Edited by: Jeff Schwartz, Griffith University, Australia

                Reviewed by: Claire Joanne Stocker, University of Buckingham, UK; Andy Levy, University of Bristol, UK; Sarah McMullen, University of Nottingham, UK

                *Correspondence: Susan E. Ozanne, Metabolic Research Laboratories, Institute of Metabolic Science, Addenbrooke’s Hospital, University of Cambridge, Cambridge CB2 0QQ, UK. e-mail: seo10@ 123456mole.bio.cam.ac.uk

                This article was submitted to Frontiers in Epigenomics, a aspecialty of Frontiers in Genetics.

                Article
                10.3389/fgene.2011.00027
                3268582
                22303323
                ce36430d-9d7e-4553-97a9-218e770a20e5
                Copyright © 2011 Alfaradhi and Ozanne.

                This is an open-access article subject to a non-exclusive license between the authors and Frontiers Media SA, which permits use, distribution and reproduction in other forums, provided the original authors and source are credited and other Frontiers conditions are complied with.

                Page count
                Figures: 2, Tables: 0, Equations: 0, References: 127, Pages: 13, Words: 12809
                Categories
                Genetics
                Review Article

                Genetics

                maternal overnutrition, epigenetics, obesity, developmental programming

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