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Glucose uptake and lipid metabolism are impaired in epicardial adipose tissue from heart failure patients with or without diabetes

2016-04-01Journal article Open access
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dc.contributor.authorBurgeiro, A
dc.contributor.authorFuhrmann, A
dc.contributor.authorCherian, S
dc.contributor.authorEspinoza, D
dc.contributor.authorJarak, I
dc.contributor.authorCarvalho, RA
dc.contributor.authorLoureiro, M
dc.contributor.authorPatrício, M
dc.contributor.authorAntunes, MJ
dc.contributor.authorCarvalho, E
dc.date.accessioned2019-05-22T16:07:20Z
dc.date.available2019-05-22T16:07:20Z
dc.date.issued2016-04-01
dc.description.abstractType 2 diabetes mellitus is a complex metabolic disease, and cardiovascular disease is a leading complication of diabetes. Epicardial adipose tissue surrounding the heart displays biochemical, thermogenic, and cardioprotective properties. However, the metabolic cross-talk between epicardial fat and the myocardium is largely unknown. This study sought to understand epicardial adipose tissue metabolism from heart failure patients with or without diabetes. We aimed to unravel possible differences in glucose and lipid metabolism between human epicardial and subcutaneous adipocytes and elucidate the potential underlying mechanisms involved in heart failure. Insulin-stimulated [(14)C]glucose uptake and isoproterenol-stimulated lipolysis were measured in isolated epicardial and subcutaneous adipocytes. The expression of genes involved in glucose and lipid metabolism was analyzed by reverse transcription-polymerase chain reaction in adipocytes. In addition, epicardial and subcutaneous fatty acid composition was analyzed by high-resolution proton nuclear magnetic resonance spectroscopy. The difference between basal and insulin conditions in glucose uptake was significantly decreased (P= 0.006) in epicardial compared with subcutaneous adipocytes. Moreover, a significant (P< 0.001) decrease in the isoproterenol-stimulated lipolysis was also observed when the two fat depots were compared, and it was strongly correlated with lipolysis, lipid storage, and inflammation-related gene expression. Moreover, the fatty acid composition of these tissues was significantly altered by diabetes. These results emphasize potential metabolic differences between both fat depots in the presence of heart failure and highlight epicardial fat as a possible therapeutic target in situ in the cardiac microenvironment.pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationAm J Physiol Endocrinol Metab. 2016 Apr 1;310(7):E550-64.pt_PT
dc.identifier.doi10.1152/ajpendo.00384.2015pt_PT
dc.identifier.urihttp://hdl.handle.net/10400.4/2222
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.subjectAdipócitospt_PT
dc.subjectTecido Adiposopt_PT
dc.subjectDiabetes Mellitus Tipo 2pt_PT
dc.subjectInsuficiência Cardíacapt_PT
dc.subjectLipólisept_PT
dc.titleGlucose uptake and lipid metabolism are impaired in epicardial adipose tissue from heart failure patients with or without diabetespt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.citation.endPageE564pt_PT
oaire.citation.issue7pt_PT
oaire.citation.startPageE550-64pt_PT
oaire.citation.volume310pt_PT
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT

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