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The conflicting effects of maternal nutrient restriction and early-life obesity on renal health.

机译:母体营养限制和早期肥胖对肾脏健康的矛盾影响。

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Epidemiological and animal studies have demonstrated that early-life nutrition alters the metabolic responses and generates structural changes in complex tissues, such as the kidneys, which may lead to a reduction in the offspring lifespan. Independently, obesity induces a spontaneous low-grade chronic inflammatory response by modulating several of the major metabolic pathways that ultimately compromise long-term renal health. However, the combined effects of maternal nutrition and early-life obesity in the development of renal diseases are far from conclusive. Previous results, using the ovine model, demonstrated that the combination of a reduction in fetal nutrition and juvenile obesity induced a series of adaptations associated with severe metabolic syndrome in the heart and adipose tissue. Surprisingly, exposure to an obesogenic environment in the kidney of those offspring produced an apparent reduction in glomerulosclerosis in relation to age- and weight-matched controls. However, this reduction in cellular apoptosis was accompanied by a rise in glomerular filtration rate and blood pressure of equal intensity when compared with obese controls. The intention of this review is to explain the adaptive responses observed in this model, based on insights into the mechanism of renal fetal programming, and their potential interactions with some of the metabolic changes produced by obesity.
机译:流行病学和动物研究表明,早期营养会改变代谢反应并在复杂组织(例如肾脏)中产生结构变化,这可能会导致后代寿命缩短。肥胖通过调节几种主要代谢途径最终导致长期肾脏健康受损,从而诱发自发性低度慢性炎症反应。然而,母体营养和早期肥胖对肾脏疾病发展的综合影响远没有定论。使用绵羊模型的先前结果表明,胎儿营养减少和青少年肥胖的组合在心脏和脂肪组织中诱发了一系列与严重代谢综合征相关的适应性疾病。出乎意料的是,与年龄和体重相称的对照组相比,这些后代在肾脏的致肥胖环境中暴露后,肾小球硬化明显减少。然而,与肥胖对照组相比,这种细胞凋亡的减少伴随着肾小球滤过率的增加和相等强度的血压的升高。这篇综述的目的是基于对肾脏胎儿编程机制的了解以及它们与肥胖引起的某些代谢变化的潜在相互作用,来解释在该模型中观察到的适应性反应。

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