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World J Diabetes. Nov 15, 2012; 3(11): 178-181
Published online Nov 15, 2012. doi: 10.4239/wjd.v3.i11.178
Gestational nutrition and the development of obesity during adulthood
Rajendra Raghow
Rajendra Raghow, Department of Veterans Affairs Medical Center, Memphis, TN 38104, United States
Rajendra Raghow, Department of Pharmacology, University of Tennessee Health Science Center, Memphis TN 38163, United States
Author contributions: Raghow R wrote the paper.
Correspondence to: Rajendra Raghow, PhD, Professor, Department of Veterans Affairs Medical Center, 1030 Jefferson Avenue, Memphis, TN 38104, United States. rraghow@uthsc.edu
Telephone: +1-901-5238990 Fax: +1-901-5237274
Received: July 18, 2012
Revised: October 26, 2012
Accepted: November 7, 2012
Published online: November 15, 2012
Abstract

Recent epidemiological studies indicate a strong link between intrauterine under-nutrition and propensity of such offspring for developing obesity and metabolic syndrome in later life. Garg et al investigated the mechanistic basis of this phenomenon and its potential reversibility in rats. The authors found that rats experiencing gestational under-nutrition but fed normally after birth (IUGR) gained body mass with excessive subcutaneous and visceral fat. The IUGR rats were also metabolically inflexible since they showed similar rates of energy expenditure and O2 consumption in the fed and fasted states. However, if such pups were food-restricted during lactation (PNGR), their metabolic profiles resembled those of control and IPGR (subject to food restriction during pre- and postnatal periods) rats. Thus, postnatal caloric restriction superimposed on intrauterine under nutrition significantly improved insulin sensitivity and adiposity of rats that would otherwise develop metabolic inflexibility and visceral obesity. The observations of Garg et al, have serious implications in term of the design of the future experimental studies as well as their clinical translation in humans.

Keywords: Intrauterine under-nutrition; Metabolic plasticity; Type 2 diabetes; Metabolic syndrome; Caloric restriction