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Endocrinology. 2012 Mar;153(3):1279-87. doi: 10.1210/en.2011-1689. Epub 2012 Jan 17.

Physiological responses to acute psychological stress are reduced by the PPARγ agonist rosiglitazone.

Author information

  • 1Department of Internal Medicine, Division of Endocrinology, Diabetes, and Metabolism, The University of Cincinnati College of Medicine, Cincinnati, Ohio 45237, USA. karen.ryan@uc.edu

Abstract

Physiological reactions to psychological stress are positively associated with several important chronic conditions including cardiovascular and neurodegenerative diseases and are linked to increased mortality. As such, the identification of cellular and molecular pathways that act to reduce stress responding may represent important targets for therapeutic intervention. Here we report that acute treatment with the peroxisome-proliferator activated receptor-γ (PPARγ) agonist rosiglitazone (RSG) blunts systemic responses to acute psychological stress in rats. Rats that had previously received oral RSG for 5 d exhibited a 40% reduction in the initial heart rate response to an acute restraint stress, compared with vehicle-treated controls, suggesting that increased PPARγ signaling blunts the acute autonomic response to stress. Rats previously treated with RSG likewise had a blunted hormonal response to this stressor, exhibiting a 30% reduction in peak corticosterone levels compared with controls. Moreover, stress-induced expression of c-Fos, a marker of early neuronal activation, was similarly reduced in the paraventricular hypothalamus, a key site for brain stress integration, facilitating both autonomic and hypothalamic-pituitary-adrenocortical responses to stress. Taken as a whole, these data suggest that PPARγ stimulation potently inhibits physiological responses to psychological stress, prescribing a novel role for PPARγ signaling in the regulation of brain stress integration.

PMID:
22253428
[PubMed - indexed for MEDLINE]
PMCID:
PMC3281543
Free PMC Article

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