Guelph Research and Development Centre, Agriculture and Agri-Food Canada, Guelph, ON N1G 5C9, Canada.
School of Pharmacy, Faculty of Medical Sciences, The University of the West Indies, St. Augustine, Trinidad and Tobago.
Nutrients. 2020 Nov 5;12(11):3404. doi: 10.3390/nu12113404.
The mechanism by which high fat-diet induced obesity affects cardiac protein expression is unclear, and the extent to which this is modulated by prebiotic treatment is not known. These outcomes were assessed in rats initially fed a high-fat diet, then the top 40% weight gain group were randomly allocated to control (CON), high-fat (HF) and HF supplemented with fructooligosaccharide (32 g; HF-FOS) treatments for 12 weeks ( = 10/group). At sacrifice, left ventricles were either frozen or preserved in formalin. Serum was stored for glucose and insulin measurements. Protein spectra was obtained using an Orbitrap analyzer, processed with Sequest and fold changes assessed with Scaffold Q +. Treatment effects for body weights, glucose and insulin were assessed using one-way ANOVA, and the differential protein expression was assessed by a Mann-Whitney U test. The Database for Annotation, Visualization and Integrated Discovery and the Kyoto Encyclopedia of Genes and Genomes identified pathways containing overrepresented proteins. Hematoxylin and eosin sections were graded for hypertrophy and also quantified; differences were identified using Chi-square analyses and Mann-Whitney U tests. HF diet fed rats were significantly ( < 0.05) heavier than CON, and 23 proteins involved in mitochondrial function and lipid metabolism were differentially expressed between HF and CON. Between HF-FOS and HF, 117 proteins involved in contractility, lipid and carbohydrate metabolism were differentially expressed. HF cardiomyocytes were significantly ( < 0.05) more hypertrophic than CON. We conclude that high-fat feeding and FOS are associated with subcellular deviations in cardiac metabolism and contractility, which may influence myocardial function and alter the risk of cardiovascular disease.
高脂肪饮食诱导的肥胖影响心脏蛋白表达的机制尚不清楚,而这种影响在多大程度上受到益生元治疗的调节也尚不清楚。这些结果在最初喂食高脂肪饮食的大鼠中进行了评估,然后将体重增加最多的前 40%的大鼠随机分配到对照组(CON)、高脂肪组(HF)和高脂肪组中补充果寡糖(32g;HF-FOS)治疗 12 周(每组 10 只)。在牺牲时,左心室要么冷冻,要么保存在福尔马林中。储存血清用于葡萄糖和胰岛素测量。使用轨道阱分析仪获得蛋白质谱,用 Sequest 进行处理,并使用 Scaffold Q + 评估折叠变化。使用单向方差分析评估体重、葡萄糖和胰岛素的治疗效果,使用曼-惠特尼 U 检验评估差异蛋白表达。数据库用于注释、可视化和综合发现和京都基因和基因组百科全书确定了包含代表性蛋白的途径。苏木精和伊红切片按肥大分级,并进行定量;使用卡方分析和曼-惠特尼 U 检验识别差异。高脂肪饮食喂养的大鼠体重明显(<0.05)高于 CON,并且在 HF 和 CON 之间有 23 种参与线粒体功能和脂质代谢的蛋白质表达不同。在 HF-FOS 和 HF 之间,有 117 种参与收缩性、脂质和碳水化合物代谢的蛋白质表达不同。HF 心肌细胞明显(<0.05)比 CON 更肥大。我们得出结论,高脂肪喂养和 FOS 与心脏代谢和收缩性的亚细胞偏差有关,这可能影响心肌功能并改变心血管疾病的风险。