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哺乳期大鼠补充肌醇可预防轻度孕期热量限制对下丘脑结构的不良编程影响,部分作用可与瘦素相当。

Myo-Inositol Supplementation in Suckling Rats Protects against Adverse Programming Outcomes on Hypothalamic Structure Caused by Mild Gestational Calorie Restriction, Partially Comparable to Leptin Effects.

机构信息

Laboratory of Molecular Biology, Nutrition and Biotechnology (Nutrigenomics and Obesity), University of the Balearic Islands, 07122 Palma, Spain.

CIBER de Fisiopatología de la Obesidad y Nutrición (CIBEROBN), 07122 Palma, Spain.

出版信息

Nutrients. 2021 Sep 18;13(9):3257. doi: 10.3390/nu13093257.

DOI:10.3390/nu13093257
PMID:34579137
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8466200/
Abstract

We studied whether myo-inositol supplementation throughout lactation, alone and combined with leptin, may reverse detrimental effects on hypothalamic structure and function caused by gestational calorie gestation (CR) in rats. Candidate early transcript-based biomarkers of metabolic health in peripheral blood mononuclear cells (PBMC) were also studied. Offspring of dams exposed to 25% gestational CR and supplemented during lactation with physiological doses of leptin (CR-L), myo-inositol (CR-M), the combination (CR-LM), or the vehicle (CR-V) as well as control rats (CON-V) were followed and sacrificed at postnatal day 25. Myo-inositol and the combination increased the number of neurons in arcuate nucleus (ARC) (only in females) and paraventricular nucleus, and myo-inositol (alone) restored the number of αMSH neurons in ARC. Hypothalamic mRNA levels of in CR-M and in CR-M and CR-LM males were higher than in CR-V and CON-V, respectively. In PBMC, increased expression levels of and in CR-V were partially normalized in all supplemented groups (but only in males for ). Therefore, myo-inositol supplementation throughout lactation, alone and combined with leptin, reverts programmed alterations by fetal undernutrition on hypothalamic structure and gene expression of potential early biomarkers of metabolic health in PBMC, which might be attributed, in part, to increased leptin sensitivity.

摘要

我们研究了在哺乳期单独补充肌醇和与瘦素联合补充是否可以逆转妊娠卡路里限制(CR)对大鼠下丘脑结构和功能的有害影响。还研究了外周血单核细胞(PBMC)中代谢健康的早期候选转录本生物标志物。暴露于 25%妊娠 CR 并在哺乳期用生理剂量的瘦素(CR-L)、肌醇(CR-M)、组合(CR-LM)或载体(CR-V)补充的母鼠的后代以及对照大鼠(CON-V)在产后 25 天被跟踪并被处死。肌醇和组合增加了弓状核(ARC)(仅在雌性中)和室旁核中神经元的数量,肌醇(单独)恢复了 ARC 中 αMSH 神经元的数量。CR-M 和 CR-M 和 CR-LM 雄性的下丘脑 mRNA 水平高于 CR-V 和 CON-V。在 PBMC 中,CR-V 中 和 的表达水平增加在所有补充组中均部分正常化(但仅在雄性中为 )。因此,哺乳期单独补充肌醇和与瘦素联合补充可以逆转胎儿营养不良对 PBMC 中代谢健康潜在早期生物标志物的下丘脑结构和基因表达的编程改变,这可能部分归因于瘦素敏感性的增加。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f07/8466200/dde75a27e88f/nutrients-13-03257-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f07/8466200/168d84f4e205/nutrients-13-03257-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f07/8466200/a91ac2652466/nutrients-13-03257-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f07/8466200/468bf540aaf9/nutrients-13-03257-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f07/8466200/dde75a27e88f/nutrients-13-03257-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f07/8466200/168d84f4e205/nutrients-13-03257-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f07/8466200/a91ac2652466/nutrients-13-03257-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f07/8466200/468bf540aaf9/nutrients-13-03257-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f07/8466200/dde75a27e88f/nutrients-13-03257-g004.jpg

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Lactation as a programming window for metabolic syndrome.哺乳期作为代谢综合征的编程窗口。
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