Mourmoura Evangelia, Chaté Valérie, Couturier Karine, Laillet Brigitte, Vial Guillaume, Rigaudiere Jean-Paul, Morio Béatrice, Malpuech-Brugère Corinne, Azarnoush Kasra, Demaison Luc
Université Joseph Fourier, Laboratoire de Bioénergétique Fondamentale et Appliquée, BP 53, Grenoble F-38041, France.
Cardiovasc Diabetol. 2014 Feb 27;13:54. doi: 10.1186/1475-2840-13-54.
Saturated fatty acid-rich high fat (HF) diets trigger abdominal adiposity, insulin resistance, type 2 diabetes and cardiac dysfunction. This study was aimed at evaluating the effects of nascent obesity on the cardiac function of animals fed a high-fat diet and at analyzing the mechanisms by which these alterations occurred at the level of coronary reserve.
Rats were fed a control (C) or a HF diet containing high proportions of saturated fatty acids for 3 months. Thereafter, their cardiac function was evaluated in vivo using a pressure probe inserted into the cavity of the left ventricle. Their heart was isolated, perfused iso-volumetrically according to the Langendorff mode and the coronary reserve was evaluated by determining the endothelial-dependent (EDV) and endothelial-independent (EIV) vasodilatations in the absence and presence of endothelial nitric oxide synthase and cyclooxygenase inhibitors (L-NAME and indomethacin). The fatty acid composition of cardiac phospholipids was then evaluated.
Although all the HF-fed rats increased their abdominal adiposity, some of them did not gain body weight (HF- group) compared to the C group whereas other ones had a higher body weight (HF+). All HF rats displayed a higher in vivo cardiac activity associated with an increased EDV. In the HF- group, the improved EDV was due to an increase in the endothelial cell vasodilatation activity whereas in the HF+ group, the enhanced EDV resulted from an improved sensitivity of coronary smooth muscle cells to nitric oxide. Furthermore, in the HF- group the main pathway implicated in the EDV was the NOS pathway while in the HF+ group the COX pathway.
Nascent obesity-induced improvement of cardiac function may be supported by an enhanced coronary reserve occurring via different mechanisms. These mechanisms implicate either the endothelial cells activity or the smooth muscle cells sensitivity depending on the body adiposity of the animals.
富含饱和脂肪酸的高脂(HF)饮食会引发腹部肥胖、胰岛素抵抗、2型糖尿病和心脏功能障碍。本研究旨在评估初发肥胖对高脂饮食喂养动物心脏功能的影响,并分析这些改变在冠状动脉储备水平上发生的机制。
将大鼠分为对照组(C)或喂食含高比例饱和脂肪酸的HF饮食3个月。此后,使用插入左心室腔的压力探头在体内评估其心脏功能。分离心脏,按照Langendorff模式进行等容灌注,并通过在不存在和存在内皮型一氧化氮合酶和环氧化酶抑制剂(L-NAME和吲哚美辛)的情况下测定内皮依赖性(EDV)和内皮非依赖性(EIV)血管舒张来评估冠状动脉储备。然后评估心脏磷脂的脂肪酸组成。
尽管所有喂食HF饮食的大鼠腹部肥胖均增加,但其中一些与C组相比体重未增加(HF-组),而其他大鼠体重更高(HF+组)。所有HF大鼠均表现出较高的体内心脏活动,伴有EDV增加。在HF-组中,EDV的改善归因于内皮细胞血管舒张活性的增加,而在HF+组中,EDV的增强是由于冠状动脉平滑肌细胞对一氧化氮的敏感性提高。此外,在HF-组中,EDV涉及的主要途径是NOS途径,而在HF+组中是COX途径。
初发肥胖诱导的心脏功能改善可能通过不同机制增强冠状动脉储备来支持。这些机制取决于动物的身体肥胖程度,涉及内皮细胞活性或平滑肌细胞敏感性。