Utilize este identificador para referenciar este registo: http://hdl.handle.net/1822/45145

TítuloGlucose intolerance after chronic stress is related with downregulated PPAR-gamma in adipose tissue
Autor(es)Pereira, Vitor H.
Marques, Fernanda
Lages, Vânia
Pereira, Filipa Gama
Patchev, Alexandre Vladimirov
Almeida, O. F. X.
Palha, Joana Almeida
Sousa, Nuno
Cerqueira, João José
Palavras-chaveChronic unpredictable stress
Glucose intolerance
Metabolic syndrome
PPAR
Lipocalin-2
White adipose tissue
Data5-Ago-2016
EditoraSpringer
RevistaCardiovascular Diabetology
Resumo(s)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.
Tipoarticle
URIhttp://hdl.handle.net/1822/45145
DOI10.1186/s12933-016-0433-2
ISSN1475-2840
Versão da editorahttp://link.springer.com
Arbitragem científicayes
AcessoopenAccess
Aparece nas coleções:ICVS - Artigos em Revistas Internacionais com Referee

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