Heart-protective effect of n-3 PUFA demonstrated in a rat model of diabetic cardiomyopathy |
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Authors: | Zhukovska Anna Shysh Angela Bacova Barbara Radosinska Jana Benova Tamara Viczenczova Csilla Dosenko Victor Moybenko Oleksiy Tribulova Narcisa |
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Affiliation: | 1. State Key Laboratory of Molecular and Cellular Biology, Bogomoletz Institute of Physiology, Kiev, Ukraine 2. Institute for Heart Research, Slovak Academy of Sciences, Dúbravská cesta 9, POBox 104, 840 05, Bratislava, Slovakia 3. Institute of Physiology, Medical Faculty of Comenius University, Bratislava, Slovakia
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Abstract: | 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. |
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