Division of Cardiology, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Taiwan; Center for Lipid Biosciences, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan; Lipid Science and Aging Research Center, Kaohsiung Medical University, Kaohsiung, Taiwan.
Division of Cardiology, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Taiwan; Department of Internal Medicine, Faculty of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan; Center for Lipid Biosciences, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan; Lipid Science and Aging Research Center, Kaohsiung Medical University, Kaohsiung, Taiwan; Research Center for Natural Products & Drug Development, Kaohsiung Medical University, Kaohsiung, Taiwan; Institute/Center of Medical Science and Technology, National Sun Yat-sen University, Kaohsiung, Taiwan.
J Formos Med Assoc. 2018 Jul;117(7):621-631. doi: 10.1016/j.jfma.2017.08.008. Epub 2017 Sep 6.
BACKGROUND/PURPOSE: Left ventricular hypertrophy is a major cause of heart failure in aging population. This study is to determine whether an excess dietary fat is lipotoxic or lipoprotein to the hypertrophic aging heart.
At 44-week-old, a normal chow (12% fat) was replaced a high-fat diet (HFD; 45% fat) for randomly selective spontaneously hypertensive rats (SHR + HFD, n = 6) and Wistar-Kyoto rats (WKY + HFD, n = 6, normotensive control). Others (SHR, n = 11; WKY, n = 10) were continuously fed with normal diets. After 27 weeks, electrocardiogram, echocardiography, and femoral arterial catheterization were performed before rats being sacrificed for molecular biology analyses.
HFD aggravated cardiac atrial, ventricular dilation and hypertrophy in SHR (LV mass: SHR + HFD 2026.0 ± 424.9 vs SHR 1449 ± 461.1 mg, unpaired t test P < 0.05). HFD caused significant atrial dilatation in both WKY (LA diameter, 5.38 ± 0.36 vs 4.11 ± 0.42 mm, P < 0.001) and SHR (6.13 ± 0.79 vs 4.69 ± 1.00, P < 0.01). Only in SHR, HFD induced significant left ventricular dilatation (LV diameter, 8.87 ± 1.25 vs 7.08 ± 1.00 mm, P < 0.01) and reduced ejection fraction (LVEF, 62.8 ± 11.6 vs 75.1 ± 9.2 mm, P < 0.05). The α-myosin heavy chain was significantly upregulated in atria and ventricles of HFD groups. HFD induced significant upregulation of PPARα, ACADM, and TNFα transcripts in atrial tissues (P < 0.05).
Hypertensive heart disease in aging rats was aggravated by HFD with worse atrial, ventricular remodeling and associated with left ventricular systolic function impairment.
背景/目的：左心室肥厚是老龄化人口心力衰竭的主要原因。本研究旨在确定过量的膳食脂肪对肥厚老化心脏是脂毒性的还是脂蛋白毒性的。
在 44 周龄时，用高脂肪饮食（HFD；45%脂肪）替代正常饲料（12%脂肪），用于随机选择的自发性高血压大鼠（SHR+HFD，n=6）和 Wistar-Kyoto 大鼠（WKY+HFD，n=6，正常血压对照）。其他（SHR，n=11；WKY，n=10）连续给予正常饮食。27 周后，在大鼠被处死进行分子生物学分析之前，进行心电图、超声心动图和股动脉导管插入术。
HFD 加重了 SHR 的心脏心房、心室扩张和肥厚（LV 质量：SHR+HFD 2026.0±424.9 与 SHR 1449±461.1 mg，未配对 t 检验 P<0.05）。HFD 导致 WKY（LA 直径，5.38±0.36 与 4.11±0.42 mm，P<0.001）和 SHR（6.13±0.79 与 4.69±1.00，P<0.01）的心房明显扩张。仅在 SHR 中，HFD 诱导明显的左心室扩张（LV 直径，8.87±1.25 与 7.08±1.00 mm，P<0.01）和射血分数降低（LVEF，62.8±11.6 与 75.1±9.2 mm，P<0.05）。α-肌球蛋白重链在 HFD 组的心房和心室中明显上调。HFD 诱导心房组织中 PPARα、ACADM 和 TNFα 转录物的显著上调（P<0.05）。
HFD 加重了老龄大鼠的高血压性心脏病，导致心房、心室重构恶化，并伴有左心室收缩功能障碍。
