INSERM U955, Université Paris-Est Creteil (UPEC), 51 Av de Lattre de Tassigny, 94100 Créteil, France.
AP-HP, Department of Cardiology, Henri Mondor Hospital, DHU-ATVB, Créteil, France.
Eur Heart J Cardiovasc Imaging. 2017 Nov 1;18(11):1283-1291. doi: 10.1093/ehjci/jew316.
Long-term high-fat diet (HFD) induces both cardiac remodelling and myocardial dysfunction in murine models. The aim was to assess the time course and mechanisms of metabolic and cardiac modifications induced by short-term HFD in wild-type (WT) mice.
Thirty-three WT mice were subjected to HFD (60% fat, n = 16) and chow diet (CD, 13% fat, n = 17). Metabolic and echocardiographic data were collected at baseline and every 5 weeks for 20 weeks. Invasive haemodynamic data and myocardial samples were collected at 5 and 20 weeks. Echocardiographic data included left ventricular (LV) diameters and thickness, and systolic function using radial strain rate (SR). Histological assessment of cardiomyocyte and adipocyte sizes, interstitial fibrosis, and apoptosis index were performed. During follow-up, body weight, and glycaemia levels were higher in HFD than in CD mice, in association with an early adipose tissue remodelling. Despite no difference between both groups in blood pressure and LV mass at 5 weeks, an early LV dysfunction was observed in HFD mice as assessed by radial SR (21 ± 0.8 vs. 27 ± 0.8 unit/s, P < 0.001) and haemodynamic assessment. During follow-up, both groups demonstrated a progressive systolic and diastolic LV dysfunction and remodelling including dilatation and hypertrophy, which were more severe in HFD mice. Compared with CD mice, the early LV impairment in HFD mice was coupled with a higher cardiomyocyte apoptosis level (0.95 vs. 0.02%, P < 0.05) associated with an interstitial fibrosis process (2.3 vs. 0.2%, P < 0.05), which worsen during follow-up.
The HFD promoted early metabolic and cardiac dysfunctions, and adipose and myocardial tissues remodelling.
长期高脂饮食(HFD)可诱导小鼠模型的心肌重构和心功能障碍。本研究旨在评估短期 HFD 对野生型(WT)小鼠代谢和心脏改变的时程和机制。
33 只 WT 小鼠分别给予 HFD(60%脂肪,n=16)和 CD(13%脂肪,n=17)。在基线和 20 周内每 5 周收集代谢和超声心动图数据。在第 5 周和第 20 周收集侵入性血流动力学数据和心肌样本。超声心动图数据包括左心室(LV)直径和厚度,以及径向应变率(SR)评估的收缩功能。对心肌细胞和脂肪细胞大小、间质纤维化和细胞凋亡指数进行组织学评估。在随访期间,HFD 组的体重和血糖水平高于 CD 组,同时脂肪组织也较早发生重塑。尽管在第 5 周时两组的血压和 LV 质量没有差异,但 HFD 组的 LV 功能较早受损,表现为径向 SR(21±0.8 与 27±0.8 单位/s,P<0.001)和血流动力学评估降低。在随访期间,两组均出现进行性 LV 收缩和舒张功能障碍及重构,包括扩张和肥大,HFD 组更为严重。与 CD 组相比,HFD 组早期 LV 损伤与更高的心肌细胞凋亡水平(0.95 与 0.02%,P<0.05)相关,同时伴有间质纤维化过程(2.3 与 0.2%,P<0.05),这在随访期间进一步恶化。
HFD 可导致早期代谢和心脏功能障碍,以及脂肪和心肌组织重塑。