Obesity is mediated by differential aryl hydrocarbon receptor signaling in mice fed a Western diet.

Document Type

Journal Article

Publication Date

9-1-2012

Journal

Environmental health perspectives

Volume

120

Issue

9

DOI

10.1289/ehp.1205003

Keywords

Adipose Tissue; Animals; Body Weight; Diet; Dietary Fats; Liver; Mice; Mice, Inbred C57BL; MicroRNAs; Models, Animal; Obesity; Polymerase Chain Reaction; RNA, Messenger; Receptors, Aryl Hydrocarbon; Signal Transduction

Abstract

BACKGROUND: Obesity is a growing worldwide problem with genetic and environmental causes, and it is an underlying basis for many diseases. Studies have shown that the toxicant-activated aryl hydrocarbon receptor (AHR) may disrupt fat metabolism and contribute to obesity. The AHR is a nuclear receptor/transcription factor that is best known for responding to environmental toxicant exposures to induce a battery of xenobiotic-metabolizing genes.

OBJECTIVES: The intent of the work reported here was to test more directly the role of the AHR in obesity and fat metabolism in lieu of exogenous toxicants.

METHODS: We used two congenic mouse models that differ at the Ahr gene and encode AHRs with a 10-fold difference in signaling activity. The two mouse strains were fed either a low-fat (regular) diet or a high-fat (Western) diet.

RESULTS: The Western diet differentially affected body size, body fat:body mass ratios, liver size and liver metabolism, and liver mRNA and miRNA profiles. The regular diet had no significant differential effects.

CONCLUSIONS: The results suggest that the AHR plays a large and broad role in obesity and associated complications, and importantly, may provide a simple and effective therapeutic strategy to combat obesity, heart disease, and other obesity-associated illnesses.

Comments

This is an open access PubMed Central article.

Peer Reviewed

1

Open Access

1

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