A SGLT2 inhibitor dapagliflozin suppresses prolonged ventricular-repolarization through augmentation of mitochondrial function in insulin-resistant metabolic syndrome rats

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DURAK A., OLĞAR Y., Degirmenci S., AKKUŞ E., TUNCAY E., Turan B.

CARDIOVASCULAR DIABETOLOGY, cilt.17, 2018 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 17
  • Basım Tarihi: 2018
  • Doi Numarası: 10.1186/s12933-018-0790-0
  • Dergi Adı: CARDIOVASCULAR DIABETOLOGY
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Anahtar Kelimeler: Diabetes, SGLT2 inhibitors, Heart function, Electrophysiology, Oxidative stress, Insulin resistance, OXIDATIVE STRESS, NA+/H+ EXCHANGER, DYSFUNCTION, HEART, EMPAGLIFLOZIN, OBESITY, CARDIOMYOCYTES, MORTALITY, ZN2+, PATHOPHYSIOLOGY
  • Ankara Üniversitesi Adresli: Evet

Özet

Background: Metabolic syndrome (MetS) is a prevalent risk factor for cardiac dysfunction. Although SGLT2-inhibitors have important cardioprotective effects in hyperglycemia, their underlying mechanisms are complex and not completely understood. Therefore, we examined mechanisms of a SGLT2-inhibitor dapagliflozin (DAPA)-related cardioprotection in overweight insulin-resistant MetS-rats comparison with insulin (INSU), behind its glucose-lowering effect.