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Grün, Felix

Current Opinion in Endocrinology, Diabetes and Obesity: October 2010 - Volume 17 - Issue 5 - p 453–459
doi: 10.1097/MED.0b013e32833ddea0
Obesity and nutrition: Edited by Caroline M. Apovian and Jeffrey I. Mechanick

Purpose of review The environmental obesogen hypothesis postulates chemical pollutants that are able to promote obesity by altering homeostatic metabolic set-points, disrupting appetite controls, perturbing lipid homeostasis to promote adipocyte hypertrophy, or stimulating adipogenic pathways that enhance adipocyte hyperplasia during development or in adults. This review focuses on recent experimental advances for candidate obesogens that target nuclear hormone receptors when a direct link between exposure, modulation of transcriptional networks and adipogenic phenotypes can be rationalized.

Recent findings Various endocrine disrupting chemicals can disrupt hormonal signaling relevant to adipose tissue biology. In this review, progress on one identified obesogen, the organotin tributyltin, will be outlined to highlight principles and novel insights into its high-affinity nuclear hormone receptor-mediated mechanism, its effects on adipocyte biology, its potential to promote long-term obesogenic changes and its epidemiological relevance. When appropriate, important results for other suspected obesogenic ligands, including bisphenol A, phthalates, polybrominated diphenyl ethers and perfluoro-compounds, will highlight corroborating principles.

Summary These examples serve to provide perspective on the potential harm that man-made obesogenic pollutants pose to human health, focus attention on areas in which knowledge remains inadequate and prompt a re-evaluation of the causative risk factors driving the current changes in obesity rates.

Center for Complex Biological Systems, University of California Irvine, Irvine, California, USA

Correspondence to Felix Grün, PhD, Center for Complex Biological Systems, University of California Irvine, Irvine, CA 92697-2280, USA Tel: +1 949 824 1100; fax: +1 949 824 6444; e-mail:

© 2010 Lippincott Williams & Wilkins, Inc.