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Glucose intolerance after chronic stress is related with downregulated PPAR-gamma in adipose tissue

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Patchev,  Alexandre
Max Planck Institute of Psychiatry, Max Planck Society;

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Almeida,  Osborne F. X.
Max Planck Institute of Psychiatry, Max Planck Society;

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Citation

Pereira, V. H., Marques, F., Lages, V., Pereira, F. G., Patchev, A., Almeida, O. F. X., et al. (2016). Glucose intolerance after chronic stress is related with downregulated PPAR-gamma in adipose tissue. CARDIOVASCULAR DIABETOLOGY, 15: 114. doi:10.1186/s12933-016-0433-2.


Cite as: http://hdl.handle.net/11858/00-001M-0000-002C-59E8-2
Abstract
Background: Chronic stress is associated with increased risk of glucose intolerance and cardiovascular diseases, albeit through undefined mechanisms. With the aim of gaining insights into the latter, this study examined the metabolic profile of young adult male rats that were exposed to chronic unpredictable stress. Methods: Young adult male rats were submitted to 4 weeks of chronic unpredictable stress and allowed to recover for 5 weeks. An extensive analysis including of morphologic, biochemical and molecular parameters was carried out both after chronic unpredictable stress and after recovery from stress. Results: After 28 days of chronic unpredictable stress (CUS) the animals submitted to this protocol displayed less weight gain than control animals. After 5 weeks of recovery the weight gain rebounded to similar values of controls. In addition, following CUS, fasting insulin levels were increased and were accompanied by signs of impaired glucose tolerance and elevated serum corticosteroid levels. This biochemical profile persisted into the post-stress recovery period, despite the restoration of baseline corticosteroid levels. The mRNA expression levels of peroxisome proliferator-activated receptor (PPAR)-gamma and lipocalin-2 in white adipose tissue were, respectively, down-and up-regulated. Conclusions: Reduction of PPAR-gamma expression and generation of a pro-inflammatory environment by increased lipocalin-2 expression in white adipose tissue may contribute to stress-induced glucose intolerance.