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Effect of peripheral administration of leptin on the renal sympathetic nerve activity in high-fat diet-related hypertensive rats.

机译:瘦素外周给药对高脂饮食相关性高血压大鼠肾交感神经活性的影响。

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摘要

A previous study of ours demonstrated that a high-fat diet (FAT) causes body fat accumulation, as well as elevation of plasma leptin level, renal sympathetic nerve activity (RSNA), and blood pressure (BP). In the study reported here, we analyzed the role of leptin in these elevations of the RSNA and BP due to FAT feeding by assessing sympathetic and cardiovascular responses to intravenous (IV) administration of leptin in rats fed either a FAT or a high-carbohydrate diet (CHO). The results showed that baseline body fat, plasma leptin level, RSNA and BP were significantly higher in the FAT group than in the CHO group, and that IV administration of leptin elevated RSNA and plasma leptin levels but lowered BP in the CHO group. However, these effects of leptin were eliminated in the FAT group. These findings suggest that FAT-fed rats which expose basal elevation of plasma leptin levels, RSNA and BP might be hyposensitive to endogenous leptin. Therefore, leptin resistance appeared obviously in FAT-induced hypertension might indicate that leptin is implicated in generating the elevation of RSNA and BP induced by long-term FAT feeding.
机译:我们先前的研究表明,高脂饮食(FAT)会导致体内脂肪蓄积,并导致血浆瘦素水平升高,肾交感神经活性(RSNA)和血压(BP)升高。在本文报道的研究中,我们通过评估饲喂FAT或高碳水化合物饮食的大鼠对静脉注射瘦素的交感和心血管反应,分析了瘦素在这些因脂肪喂养引起的RSNA和BP升高中的作用(CHO)。结果显示,FAT组的基线人体脂肪,血浆瘦素水平,RSNA和BP均显着高于CHO组,而静脉注射瘦素可使CHO组的RSNA和血浆瘦素水平升高,但BP降低。但是,在FAT组中消除了瘦素的这些作用。这些发现表明,以脂肪喂养的大鼠暴露了血浆瘦素水平,RSNA和BP的基础升高,可能对内源性瘦素敏感。因此,瘦素抵抗在FAT诱发的高血压中明显出现,这可能表明瘦素与长期FAT喂养引起的RSNA和BP升高有关。

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