Metabolic effects of carvedilol through beta-arrestin proteins: investigations in a streptozotocin-induced diabetes rat model and in C2C12 myoblasts

GÜVEN B., Kara Z., BEŞİKCİ A.

BRITISH JOURNAL OF PHARMACOLOGY, cilt.177, sa.24, ss.5580-5594, 2020 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 177 Sayı: 24
  • Basım Tarihi: 2020
  • Doi Numarası: 10.1111/bph.15269
  • Dergi Adı: BRITISH JOURNAL OF PHARMACOLOGY
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, Agricultural & Environmental Science Database, BIOSIS, CAB Abstracts, Chemical Abstracts Core, Chimica, CINAHL, EMBASE, MEDLINE, Veterinary Science Database
  • Sayfa Sayıları: ss.5580-5594
  • Anahtar Kelimeler: beta arrestin, biased agonist, carvedilol, substrate metabolism, CHRONIC HEART-FAILURE, MITOCHONDRIAL BIOGENESIS, CARDIAC-FUNCTION, CONCISE GUIDE, INSULIN, DYSFUNCTION, ANTIOXIDANT, METOPROLOL, SENSITIVITY, MECHANISMS
  • Ankara Üniversitesi Adresli: Evet

Özet

Background and Purpose Carvedilol is a third-generation beta-adrenoceptor antagonist, which also stimulates beta-arrestins. beta-arrestins initiate intracellular signalling and are involved in insulin release and sensitivity. Carvedilol is superior in effectiveness to other drugs that are used for similar indications and does not cause insulin resistance or diabetes, which can occur with other beta-antagonists. We have shown that carvedilol increased glucose usage in C2C12 cells. We investigate the biased agonist efficacy of carvedilol on beta-arrestins.