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Impact of stress and stress physiology during pregnancy on child metabolic function and obesity risk

Entringer, Sonja

Current Opinion in Clinical Nutrition & Metabolic Care: May 2013 - Volume 16 - Issue 3 - p 320–327
doi: 10.1097/MCO.0b013e32835e8d80
PAEDIATRICS: Edited by Berthold Koletzko and Raanan Shamir

Purpose of review To summarize recent conceptual frameworks and empirical findings addressing the role of prenatal stress and stress biology in the context of fetal programming of metabolic function and obesity risk.

Recent findings The link between stress exposure and adverse health outcomes is well established. Growing evidence from animal and human studies now suggests that the experience of severe stress or perturbations in stress-related immune and endocrine processes during pregnancy may also impact the developing fetus to produce increased susceptibility for childhood and adult obesity, and dysregulated glycemic control.

Summary Because endocrine and immune ligands commonly associated with stress play an essential role during intrauterine development in cellular growth and differentiation perturbations in these systems during pregnancy are likely to produce alterations of structure and function of the brain and peripheral physiological systems in the offspring. To systematically study the effects of intrauterine stress exposure on child metabolic function and obesity risk, a multilevel approach is required that includes molecular and cellular studies, the use of animal models, and human observational and interventional studies. Such studies will set the stage for translational research to inform the subsequent development of diagnostic and primary or secondary intervention strategies in at-risk individuals.

Department of Pediatrics, University of California, Irvine, California, USA

Correspondence to Sonja Entringer, PhD, UC Irvine Development, Health and Disease Research Program, University of California, Irvine, 333 The City Blvd. W, Suite 1200 Orange, CA 92868, USA. Tel: +1 714 940 1924; fax: +1 714 940 1939; e-mail:

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