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Impaired mitochondrial oxidative phosphorylation capacity in epicardial adipose tissue is associated with decreased concentration of adiponectin and severity of coronary atherosclerosis

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  • Takayuki Nakajima
  • Takashi Yokota
  • Yasushige Shingu
  • Akira Yamada
  • Yutaka Iba
  • Kosuke Ujihira
  • Satoru Wakasa
  • Tomonori Ooka
  • Shingo Takada
  • Ryosuke Shirakawa
  • Takashi Katayama
  • Takaaki Furihata
  • Arata Fukushima
  • Ryosuke Matsuoka
  • Hiroshi Nishihara
  • Flemming Dela
  • Katsuhiko Nakanishi
  • Yoshiro Matsui
  • Shintaro Kinugawa
Vis graf over relationer

Epicardial adipose tissue (EAT), a source of adipokines, is metabolically active, but the role of EAT mitochondria in coronary artery disease (CAD) has not been established. We investigated the association between EAT mitochondrial respiratory capacity, adiponectin concentration in the EAT, and coronary atherosclerosis. EAT samples were obtained from 25 patients who underwent elective cardiac surgery. Based on the coronary angiographycal findings, the patients were divided into two groups; coronary artery disease (CAD; n = 14) and non-CAD (n = 11) groups. The mitochondrial respiratory capacities including oxidative phosphorylation (OXPHOS) capacity with non-fatty acid (complex I and complex I + II-linked) substrates and fatty acids in the EAT were significantly lowered in CAD patients. The EAT mitochondrial OXPHOS capacities had a close and inverse correlation with the severity of coronary artery stenosis evaluated by the Gensini score. Intriguingly, the protein level of adiponectin, an anti-atherogenic adipokine, in the EAT was significantly reduced in CAD patients, and it was positively correlated with the mitochondrial OXPHOS capacities in the EAT and inversely correlated with the Gensini score. Our study showed that impaired mitochondrial OXPHOS capacity in the EAT was closely linked to decreased concentration of adiponectin in the EAT and severity of coronary atherosclerosis.

OriginalsprogEngelsk
TidsskriftScientific Reports
Vol/bind9
Udgave nummer1
Sider (fra-til)3535
ISSN2045-2322
DOI
StatusUdgivet - 5 mar. 2019

ID: 56875314