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首页> 外文期刊>Mediators of inflammation >Dietary Supplemental Glutamine Enhances the Percentage of Circulating Endothelial Progenitor Cells in Mice with High-Fat Diet-Induced Obesity Subjected to Hind Limb Ischemia
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Dietary Supplemental Glutamine Enhances the Percentage of Circulating Endothelial Progenitor Cells in Mice with High-Fat Diet-Induced Obesity Subjected to Hind Limb Ischemia

机译:膳食补充谷氨酰胺提高了小鼠循环内皮祖细胞的百分比,高脂饮食诱导肥胖对后肢缺血进行后血症

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This study investigated whether glutamine (GLN) pretreatment can enhance circulating endothelial progenitor cells (EPCs) and attenuate inflammatory reaction in high-fat diet-induced obese mice with limb ischemia. Mice were assigned to a normal control (NC), high-fat control (HC), limb ischemia (HI), and GLN limb ischemia (HG) groups. The NC group provided chow diet and treated as a negative control. Mice in the HC and HI groups were fed a high-fat diet which 60% energy provided by fat for 8 weeks. Mice in the HG group were fed the same diet for 4 weeks and then transferred to a high-fat diet with 25% of total protein nitrogen provided as GLN to replace part of the casein for the subsequent 4 weeks. After feeding 8 weeks, mice in the HC group were sham-operated, while the HI and HG groups underwent an operation to induce limb ischemia. All mice except the NC group were euthanized on either day 1 or 7 after the operation. The results showed that the 8 weeks’ high-fat diet feeding resulted in obesity. The HG group had higher circulating EPCs on day 1 while muscle vascular endothelial growth factor, matrix metalloproteinase-9, and hypoxia-inducible factor-1 gene expressions were higher on day 7 postischemia than those of the HI group. The superoxide dismutase activity and reduced glutathione content in affected muscles were higher, whereas mRNA expressions of interleukin-6 and tumor necrosis factor-α were lower in the HG than those in the HI group. These findings suggest that obese mice pretreated with GLN-supplemented high-fat diet increased circulating EPC percentage, enhanced the antioxidant capacity, and attenuated inflammatory reactions in response to limb ischemia.
机译:本研究研究了谷氨酰胺(GLN)预处理是否可以增强循环内皮祖细胞(EPC),并用肢体缺血衰减高脂饮食诱导的肥胖小鼠的炎症反应。将小鼠分配给正常对照(NC),高脂肪对照(HC),肢体缺血(HI)和GLN肢体缺血(HG)组。 NC组提供了味道饮食并视为阴性对照。 HC和HI组中的小鼠喂养高脂饮食,其中脂肪提供60%的能量8周。小鼠HG组饲喂相同的饮食4周,然后转移到高脂肪的饮食与作为GLN提供总蛋白氮的25%来代替酪蛋白的部分用于随后的4周。在喂食8周后,HC组中的小鼠被假手动,而HI和HG组接受了诱导肢体缺血的操作。除了NC组外的所有小鼠在操作后1或7天安乐死。结果表明,8周的高脂饮食喂养导致肥胖。 HG组在第1天进行循环EPCS,而肌血管内皮生长因子,基质金属蛋白酶-9和缺氧诱导因子-1基因表达在第7天的产后率高于HI群体。受影响的肌肉中的超氧化物歧化酶活性和降低的谷胱甘肽含量较高,而在Hg中的白细胞介素-6和肿瘤坏死因子-α的mRNA表达比HI基团中的肿瘤坏死因子-α更低。这些研究结果表明,肥胖小鼠用Gln补充的高脂饮食预处理增加循环EPC百分比,增强了抗氧化能力,并响应于肢体缺血而减弱的炎症反应。

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