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母鼠补充牛磺酸可部分预防早期生活蛋白缺乏对β细胞功能和胰岛素敏感性的不良影响。

Maternal taurine supplementation in rats partially prevents the adverse effects of early-life protein deprivation on β-cell function and insulin sensitivity.

机构信息

Department of Physiology, University of Toronto, Toronto, Ontario, Canada.

出版信息

Reproduction. 2013 May 21;145(6):609-20. doi: 10.1530/REP-12-0388. Print 2013 Jun.

Abstract

Dietary protein restriction during pregnancy and lactation in rats impairs β-cell function and mass in neonates and leads to glucose intolerance in adult offspring. Maternal taurine (Tau) supplementation during pregnancy in rats restores β-cell function and mass in neonates, but its long-term effects are unclear. The prevention of postnatal catch-up growth has been suggested to improve glucose tolerance in adult offspring of low-protein (LP)-fed mothers. The objective of this study was to examine the relative contribution of β-cell dysfunction and insulin resistance to impaired glucose tolerance in 130-day-old rat offspring of LP-fed mothers and the effects of maternal Tau supplementation on β-cell function and insulin resistance in these offspring. Pregnant rats were fed i) control, ii) LP, and iii) LP+Tau diets during gestation and lactation. Offspring were given a control diet following weaning. A fourth group consisting of offspring of LP-fed mothers, maintained on a LP diet following weaning, was also studied (LP-all life). Insulin sensitivity in the offspring of LP-fed mothers was reduced in females but not in males. In both genders, LP exposure decreased β-cell function. Tau supplementation improved insulin sensitivity in females and β-cell function in males. The LP-all life diet improved β-cell function in males. We conclude that i) maternal Tau supplementation has persistent effects on improving glucose metabolism (β-cell function and insulin sensitivity) in adult rat offspring of LP-fed mothers and ii) increasing the amount of protein in the diet of offspring adapted to a LP diet after weaning may impair glucose metabolism (β-cell function) in a gender-specific manner.

摘要

孕期和哺乳期大鼠的蛋白质限制饮食会损害新生儿的β细胞功能和数量,并导致成年后代的葡萄糖耐量受损。孕期给大鼠补充牛磺酸(Tau)可以恢复新生儿的β细胞功能和数量,但长期效果尚不清楚。有人提出,预防出生后追赶性生长可以改善低蛋白(LP)喂养母亲的成年后代的葡萄糖耐量。本研究的目的是研究 LP 喂养母亲的后代在 130 日龄时葡萄糖耐量受损与β细胞功能障碍和胰岛素抵抗的相对关系,以及母体 Tau 补充对这些后代的β细胞功能和胰岛素抵抗的影响。孕期和哺乳期,将怀孕的大鼠分别喂食 i)对照、ii)LP 和 iii)LP+Tau 饮食。断奶后,后代给予对照饮食。还研究了一组由 LP 喂养母亲的后代组成的第四组,这些后代在断奶后继续喂食 LP 饮食(LP-终生)。LP 喂养母亲的后代的胰岛素敏感性在雌性中降低,但在雄性中没有降低。在两种性别中,LP 暴露都降低了β细胞功能。Tau 补充改善了雌性的胰岛素敏感性和雄性的β细胞功能。LP-终生饮食改善了雄性的β细胞功能。我们得出结论,i)母体 Tau 补充对改善 LP 喂养母亲的成年后代的葡萄糖代谢(β细胞功能和胰岛素敏感性)具有持久作用,ii)增加适应 LP 饮食的后代饮食中的蛋白质含量可能会以性别特异性的方式损害葡萄糖代谢(β细胞功能)。

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