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母体蛋白质限制会增加幼鼠肝脏中的糖原储备。

Maternal protein restriction increases hepatic glycogen storage in young rats.

作者信息

Gosby Alison K, Maloney Christopher A, Phuyal Jenny L, Denyer Gareth S, Bryson Janet M, Caterson Ian D

机构信息

Human Nutrition Unit, School of Molecular and Microbial Biosciences, University of Sydney, Sydney NSW 2006, Australia.

出版信息

Pediatr Res. 2003 Sep;54(3):413-8. doi: 10.1203/01.PDR.0000077470.63060.9B. Epub 2003 Jun 4.

DOI:10.1203/01.PDR.0000077470.63060.9B
PMID:12788979
Abstract

This study aimed to determine whether maternal protein restriction alters hepatic glycogen metabolism. Mated female rats were fed diets containing 20% protein throughout pregnancy and lactation (CONT), 8% protein throughout pregnancy and lactation (LP), or 8% protein during the last week of pregnancy only and lactation (LLP). Weights and lengths were reduced in the LLP and LP offspring compared with the CONT offspring. The LLP and LP offspring demonstrated reduced insulin concentrations at both 10 and 26 d and also failed to show the increase in insulin seen with time in the CONT offspring. Serum glucose and leptin levels increased with time but were not different among the groups; however, in relation to adiposity leptin levels were greater in the LLP and LP offspring at 26 d. The LLP and LP offspring had increased hepatic glycogen at day 10 (CONT, 75.1 +/- 9.8; LLP, 103.4 +/- 11.0; LP, 116.0 +/- 18.4 glucose residues/g tissue) and d 26 (CONT, 183.1 +/- 38.9; LLP, 395.3 +/- 16.8; LP, 396.6 +/- 15.1 glucose residues/g tissue). Glycogen synthase expression was increased in the LLP and LP offspring at 10 d but not 26 d; glucose transporter 2 and glycogen phosphorylase expressions were not different at either time. At 26 d glycogen synthase activity was not different; however, glycogen phosphorylase a activity was reduced. The enhanced capacity to store glycogen despite reductions in insulin secretion suggests increased insulin sensitivity possibly acting with an alternative non-insulin-dependent glycogen storage mechanism.

摘要

本研究旨在确定母体蛋白质限制是否会改变肝脏糖原代谢。将交配后的雌性大鼠在整个怀孕和哺乳期饲喂含20%蛋白质的饮食(对照组)、整个怀孕和哺乳期饲喂8%蛋白质的饮食(低蛋白组)或仅在怀孕最后一周和哺乳期饲喂8%蛋白质的饮食(晚期低蛋白组)。与对照组后代相比,晚期低蛋白组和低蛋白组后代的体重和体长降低。晚期低蛋白组和低蛋白组后代在10日龄和26日龄时胰岛素浓度均降低,且未表现出对照组后代随时间出现的胰岛素增加情况。血清葡萄糖和瘦素水平随时间升高,但各组间无差异;然而,就肥胖程度而言,晚期低蛋白组和低蛋白组后代在26日龄时的瘦素水平更高。晚期低蛋白组和低蛋白组后代在第10天(对照组,75.1±9.8;晚期低蛋白组,103.4±11.0;低蛋白组,116.0±18.4葡萄糖残基/克组织)和第26天(对照组,183.1±38.9;晚期低蛋白组,395.3±16.8;低蛋白组,396.6±15.1葡萄糖残基/克组织)时肝脏糖原增加。糖原合酶表达在晚期低蛋白组和低蛋白组后代10日龄时增加,但在26日龄时未增加;葡萄糖转运蛋白2和糖原磷酸化酶表达在两个时间点均无差异。在26日龄时糖原合酶活性无差异;然而,糖原磷酸化酶a活性降低。尽管胰岛素分泌减少,但糖原储存能力增强,这表明胰岛素敏感性增加,可能与另一种非胰岛素依赖性糖原储存机制共同起作用。

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