Details

Autor(en) / Beteiligte

• Anna, Zhukovska
• Angela, Shysh
• Barbara, Bacova
• Jana, Radosinska
• Tamara, Benova
• Csilla, Viczenczova
• Victor, Dosenko
• Oleksiy, Moybenko
• Narcisa, Tribulova

Titel

Heart-protective effect of n-3 PUFA demonstrated in a rat model of diabetic cardiomyopathy

Ist Teil von

• Molecular and cellular biochemistry, 2014-04, Vol.389 (1-2), p.219-227

Ort / Verlag

Boston: Springer US

Erscheinungsjahr

2014

Quelle

2022 ECC(Springer)

Beschreibungen/Notizen

• This study was designed to examine in vivo functional changes of the heart in the early stages of streptozotocin (STZ)-induced diabetic cardiomyopathy and to evaluate the effects of n-3 PUFA intake. Moreover, we investigated whether modulation of diabetes-related abnormalities of myocardial connexin-43 (Cx43), β-myosin heavy chain (β-MHC), and β1-adrenergic receptors (β1-AR) might be implicated in the cardioprotective mechanism of n-3 PUFA. Our results showed significantly reduced cardiac output and ejection fraction (using the microtip pressure–volume catheter technique) as well as stroke volume and stroke work, 4 weeks after STZ-induced diabetes, with improvement of these parameters due to n-3 PUFA consumption. Myocardial expression of Cx43 mRNA estimated by real-time polymerase chain reaction did not change in diabetic rats regardless of n-3 PUFA consumption (100 mg/100 g b.w./day). In contrast, the total and functional phosphorylated form of Cx43 protein increased significantly, and its cardiomyocyte-related distribution was disordered in the diabetic heart, but these changes normalized because of n-3 PUFA intake. Furthermore, acute diabetes was accompanied by decrease of myocardial β1-AR mRNA expression and mild yet nonsignificant increase of β-MHC mRNA. These alterations were not significantly affected by n-3 PUFA. In conclusion, the results point out that STZ-diabetic rats benefit from n-3 PUFA consumption particularly because of the attenuation of myocardial Cx43 abnormalities that most likely contributes to improvement of cardiac function.