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携带胎盘特异性Igf2转录本靶向破坏的胎儿的怀孕小鼠,其胎盘葡萄糖转运率增加,但与循环葡萄糖浓度升高无关。

Increased placental glucose transport rates in pregnant mice carrying fetuses with targeted disruption of their placental-specific Igf2 transcripts are not associated with raised circulating glucose concentrations.

作者信息

Petry Clive J, Evans Mark L, Wingate Dianne L, Ong Ken K, Reik Wolf, Constância Miguel, Dunger David B

机构信息

Department of Paediatrics, University of Cambridge, Box 116, Addenbrooke's Hospital, Hills Road, Cambridge CB2 0QQ, UK.

出版信息

Exp Diabetes Res. 2011;2011:171376. doi: 10.1155/2011/171376. Epub 2011 Feb 8.

DOI:10.1155/2011/171376
PMID:21331382
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3038613/
Abstract

At the beginning of the third week of pregnancy, mouse fetuses with targeted disruption of their paternally-transmitted insulin-like growth factor 2 gene placental-specific transcripts have growth-restricted placentas but normal body weights due to upregulated placental nutrient transport. We assessed whether increased placental glucose transport rates were associated with raised maternal glucose concentrations by performing intraperitoneal glucose tolerance tests (ipGTT) in pregnant mice carrying knockout pups and comparing them with mice carrying genotype-matched phenotypically wild type pups. Mean ± SD body weights of affected pups were 95 ± 8% of control values at e16 and 73 ± 7% at e18. There were no differences in areas under the maternal ipGTT curves at either e16 (mean ± SD being 99.0 ± 9.1% of control values; P = .9) or e18 (91.4 ± 13.4%; P = .3), suggesting that effects on transplacental glucose transport in these mice are not mediated through changes in maternal glucose concentrations.

摘要

在怀孕第三周开始时,父源传递的胰岛素样生长因子2基因胎盘特异性转录本被靶向破坏的小鼠胎儿,其胎盘生长受限,但由于胎盘营养物质转运上调,体重正常。我们通过对怀有基因敲除幼崽的怀孕小鼠进行腹腔葡萄糖耐量试验(ipGTT),并将它们与怀有基因型匹配的表型野生型幼崽的小鼠进行比较,来评估胎盘葡萄糖转运速率的增加是否与母体葡萄糖浓度升高有关。在胚胎第16天(e16),受影响幼崽的平均体重±标准差为对照值的95±8%,在胚胎第18天(e18)为73±7%。在e16(平均±标准差为对照值的99.0±9.1%;P = 0.9)或e18(91.4±13.4%;P = 0.3)时,母体ipGTT曲线下面积均无差异,这表明这些小鼠中对胎盘葡萄糖转运的影响不是通过母体葡萄糖浓度的变化介导的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69f1/3038613/42eb84ca60a7/EDR2011-171376.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69f1/3038613/768fa69fba2a/EDR2011-171376.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69f1/3038613/81f8ba917118/EDR2011-171376.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69f1/3038613/42eb84ca60a7/EDR2011-171376.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69f1/3038613/768fa69fba2a/EDR2011-171376.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69f1/3038613/81f8ba917118/EDR2011-171376.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69f1/3038613/42eb84ca60a7/EDR2011-171376.003.jpg

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