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Developmental Programming of Offspring Obesity, Adipogenesis, and Appetite

ROSS, MICHAEL G. MD, MPH*,†; DESAI, MINA MSc, PhD*,†

Clinical Obstetrics and Gynecology: September 2013 - Volume 56 - Issue 3 - p 529–536
doi: 10.1097/GRF.0b013e318299c39d
Fetal Origins of Adult Disease

A newly recognized primary cause of the obesity epidemic is the developmental programming effects of infants born to mothers with obesity or gestational diabetes, intrauterine growth–restricted newborns, and offspring exposed to environmental toxins including bisphenol A. The mechanisms which result in offspring obesity include the programming of the hypothalamic appetite pathway and adipogenic signals regulating lipogenesis. Processes include nutrient sensors, epigenetic modifications, and alterations in stem cell precursors of both appetite/satiety neurons and adipocytes which are modulated to potentiate offspring obesity. Future strategies for the prevention and therapy of obesity must address programming effects of the early life environment.

*Perinatal Research Laboratories, Department of Obstetrics and Gynecology, David Geffen School of Medicine, University of California, Los Angeles;

Department of Ob/Gyn, Los Angeles Biomedical Research Institute, Harbor-UCLA Medical Center, Torrance, California

Supported by the National Institutes of Health Grants R01DK081756 and R01HD054751.

The authors declare that they have nothing to disclose.

Correspondence: Michael G. Ross, MD, MPH, Department of Ob/Gyn, Los Angeles Biomedical Research Institute, Harbor-UCLA Medical Center, P.O. Box 467, Torrance, CA. E-mail: mikeross@ucla.edu

© 2013 by Lippincott Williams & Wilkins.