Sex Differences and Diabetes Mellitus in Cardiovascular Function

ÖZDEMİR S., YARAŞ N., TURAN B.

DIABETIC CARDIOMYOPATHY: BIOCHEMICAL AND MOLECULAR MECHANISMS, cilt.9, ss.159-176, 2014 (SCI-Expanded) identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 9
  • Basım Tarihi: 2014
  • Doi Numarası: 10.1007/978-1-4614-9317-4_9
  • Dergi Adı: DIABETIC CARDIOMYOPATHY: BIOCHEMICAL AND MOLECULAR MECHANISMS
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED)
  • Sayfa Sayıları: ss.159-176
  • Anahtar Kelimeler: Diabetes, Gender differences, Action potential, Ion channels, Contraction, Ca homeostasis, Oxidative stress, LEFT-VENTRICULAR DYSFUNCTION, INDUCED CARDIAC DYSFUNCTION, GENDER-RELATED DIFFERENCES, RENIN-ANGIOTENSIN SYSTEM, OXIDATIVE STRESS, RAT-HEART, RYANODINE RECEPTOR, DIASTOLIC DYSFUNCTION, ANTIOXIDANT DEFENSES, CONTRACTILE FUNCTION
  • Akdeniz Üniversitesi Adresli: Evet

Özet

Diabetes is an increasingly widespread epidemic disease, with type 2 diabetes accounting for most of the cases. Cardiovascular complications are the most common cause of morbidity and mortality in diabetic patients. Some studies have also reported that gender difference has a profound impact in the pathogenesis, development, and severity of cardiovascular diseases in diabetic patients, although this assertion was not documented and reviewed in detail. Indeed, cardiovascular diseases are the leading cause of death among women in developed countries. Similarly, results of human and animal studies have shown that sex differences cannot be ruled out in diabetes-induced cardiovascular abnormalities. The proposed underlying mechanisms of gender-related differences in response to different stimuli in healthy and diabetic subjects are the distinction in regulation of cytosolic Ca2+ levels and the varied rate of oxidative damage. The female rat myocardium is more resistant to diabetes-induced cardiac dysfunction than that of male rats, but this female advantage is canceled in postmenopausal individuals. Therefore, it is possible to suggest that estrogen can exert protective effects against diabetes through modulation of altered Ca2+ dynamics and reduction of oxidative damage in the heart. Although the current findings provide convincing evidence about the sex-related differences in diabetes-induced cardiovascular pathology, further studies are needed to clarify the underlying mechanisms of this distinction.