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母体膳食铬限制程序肌肉发育和功能的大鼠后代。

Maternal dietary chromium restriction programs muscle development and function in the rat offspring.

机构信息

National Institute of Nutrition, Hyderabad, India.

出版信息

Exp Biol Med (Maywood). 2010 Mar;235(3):349-55. doi: 10.1258/ebm.2009.009199.

DOI:10.1258/ebm.2009.009199
PMID:20404053
Abstract

Intrauterine growth retardation programs the fetus to manipulated metabolic changes that lead to adult diseases. Considering that chromium (Cr) supplements influence lean body mass (LBM) in both humans and experimental animals, we have studied the effect of maternal Cr restriction on muscle development and function in the rat offspring. Female weanling Wistar/NIN rats received, for 12 weeks, a control or 65% Cr-restricted diet ad libitum and mated with control males. While control mothers/offspring received control diet throughout (CrC), some restricted mothers were switched to control diet from conception (CrRC) and parturition (CrRP) and their offspring were weaned on to control diet. Half of the remaining restricted pups were weaned on to control diet (CrRW) and the other half continued on restricted diet throughout (CrR). Maternal CrR significantly decreased the percent of LBM (LBM %) and fat-free mass (FFM %) in the offspring and this was associated with decreased expression of the myogenic genes: MyoD, Myf5 and MyoG. Surprisingly, expression of the muscle atrophy genes, Atrogin and MuRF 1, was also decreased in CrR offspring. Although basal glucose uptake by muscle was higher in CrR than in CrC offspring, the stimulation with insulin was comparable, implying no change in its insulin sensitivity. Rehabilitation partly corrected myogenic and atrophic gene expression but had no effect on LBM % or FFM % or glucose uptake by muscle. The results show that maternal Cr restriction in rats may irreversibly impair muscle development and glucose uptake by muscle. Modulation of muscle atrophy appears to be an adaptive mechanism to preserve muscle mass in CrR offspring.

摘要

宫内生长迟缓使胎儿发生代谢变化,从而导致成年疾病。考虑到铬 (Cr) 补充剂会影响人类和实验动物的瘦体质量 (LBM),我们研究了母体 Cr 限制对大鼠后代肌肉发育和功能的影响。雌性断奶 Wistar/NIN 大鼠自由摄取对照或 65%Cr 限制饮食 12 周,并与对照雄性交配。虽然对照母亲/后代在整个过程中都接受对照饮食 (CrC),但一些限制母亲从受孕 (CrRC) 和分娩 (CrRP) 开始转换为对照饮食,并将其后代断奶至对照饮食。一半的剩余限制幼崽被断奶至对照饮食 (CrRW),另一半则继续接受限制饮食 (CrR)。母体 CrR 显著降低了后代的 LBM(LBM%)和无脂肪组织(FFM%)的比例,这与肌源性基因的表达减少有关:MyoD、Myf5 和 MyoG。令人惊讶的是,CrR 后代的肌肉萎缩基因 Atrogin 和 MuRF1 的表达也减少了。尽管 CrR 后代的肌肉基础葡萄糖摄取高于 CrC 后代,但胰岛素刺激的葡萄糖摄取相当,表明其胰岛素敏感性没有变化。康复部分纠正了肌源性和萎缩基因的表达,但对 LBM%或 FFM%或肌肉葡萄糖摄取没有影响。结果表明,大鼠母体 Cr 限制可能会不可逆地损害肌肉发育和肌肉对葡萄糖的摄取。肌肉萎缩的调节似乎是一种适应性机制,可在 CrR 后代中维持肌肉质量。

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