alexa Is the Fetal Origins Hypothesis of Diabetes Supported b
ISSN: 2155-6156

Journal of Diabetes & Metabolism
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Review Article

Is the Fetal Origins Hypothesis of Diabetes Supported by Animal Research? A Systematic Review and Meta-Analysis of the Evidence

Veenendaal MVE1*, Thangaratinam S2, Yates D3, Painter RC4, de Rooij SR1, van der Post JAM4, PMM Bossuyt1, Saade GR5, Mol BWJ4, Khan KS6 and Roseboom TJ1,4

1Department of Clinical Epidemiology, Biostatistics and Bioinformatics, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands

2Department of Obstetrics and Gynaecology and Clinical Epidemiology, University of Birmingham, Birmingham, UK

3Library and Information Service, Birmingham Women’s NHS Foundation Trust, Birmingham, UK

4Department of Obstetrics and Gynaecology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands

5Division of Maternal-Fetal Medicine, The University of Texas Medical Branch, Galveston, Texas, USA

6Barts and the London School of Medicine, London, UK

*Corresponding Author:
Marjolein Veenendaal
Department of Clinical Epidemiology
Biostatistics and Bioinformatics
Academic Medical Center, University of Amsterdam
PO box 22660, 1100 DD Amsterdam, The Netherlands
Tel: 31 20 5665810
Fax: 31 20 6912683
E-mail: [email protected]

Received date: August 27, 2013; Accepted date: November 08, 2013; Published date: November 14, 2013

Citation: Veenendaal MVE, Thangaratinam S, Yates D, Painter RC, de Rooij SR, et al. (2013) Is the Fetal Origins Hypothesis of Diabetes Supported by Animal Research? A Systematic Review and Meta-Analysis of the Evidence. J Diabetes Metab 4:307. doi: 10.4172/2155-6156.1000307

Copyright: © 2013 Veenendaal MVE, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.



The fetal programming hypothesis states that fetal undernutrition during pregnancy results in permanent changes in the offspring’s metabolism. A large number of animal studies have evaluated the effect of prenatal undernutrition on later glucose metabolism.

Aim: We systematically reviewed the existing animal literature examining effects of prenatal undernutrition on glucose and insulin metabolism.

Methods: An electronic search was performed in Medline and Embase to identify all articles that reported studies investigating the effect of prenatal undernutrition on plasma insulin, plasma glucose and beta cell mass in animal models. Summary estimates of the effect of prenatal undernutrition on mean glucose concentration, insulin level, and beta cell mass were obtained through meta-analysis.

Results: The search resulted in 1827 articles, of which 117 were potentially eligible, based on title and abstract, and 49 met the selection criteria and were included in the review. Prenatal protein restriction (but not general undernutrition) increased plasma glucose concentrations (0.42 mmol/l (95% CI 0.07 to 0.77)). Both prenatal general undernutrition and protein restriction reduced plasma insulin concentrations (general undernutrition: -0.03 nmol/l (95% CI -0.04 to -0.01), protein restricted: -0.04 nmol/l (95% CI -0.08 to 0.00)) and beta cell mass (general undernutrition: -1.24 mg (95% CI -1.88 to -0.60), protein restriction: -0.99 mg (95% CI -1.67 to -0.31)). In all cases, heterogeneity was significant.

Conclusions: Despite significant heterogeneity, evidence from experiments in different species suggests that prenatal undernutrition – both general or protein restriction – results in increased glucose and reduced insulin concentrations as well as beta cell mass in later life.


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