Evidence map›Paper›PMID 27517955›Full record

ArticleNutrients2016

Effects of Maternal Chromium Restriction on the Long-Term Programming in MAPK Signaling Pathway of Lipid Metabolism in Mice.

Qian Zhang, Xiaofang Sun, Xinhua Xiao, Jia Zheng, Ming Li, Miao Yu, Fan Ping, Zhixin Wang, Cuijuan Qi, Tong Wang and 1 more

Open access · goldAbstract read
In one paragraph

Article in Nutrients, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.7field-weighted citation impact, top 15% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

7 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Review
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  4. Article
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  6. Article
  7. Gene expression shifts in yellow-bellied marmots prior to natal dispersal.Behavioral ecology : official journal of the International Society for Behavioral Ecology
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 3 institutions in 1 country.

Qian ZhangKey Laboratory of Endocrinology, Ministry of Health, Translational Medical Center, Department of Endocrinology, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing 100730, China. zhangqian6088@pumch.cn.
Xiaofang SunDepartment of Endocrinology, The Affiliated Hospital of Qingdao University, Qingdao 266003, China. sunxiaofangpu@sohu.com.
Xinhua XiaoKey Laboratory of Endocrinology, Ministry of Health, Translational Medical Center, Department of Endocrinology, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing 100730, China. xiaoxh2014@vip.163.com.
Jia ZhengKey Laboratory of Endocrinology, Ministry of Health, Translational Medical Center, Department of Endocrinology, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing 100730, China. zhengjia_pumch@sohu.com.
Ming LiKey Laboratory of Endocrinology, Ministry of Health, Translational Medical Center, Department of Endocrinology, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing 100730, China. liming_pumch@sohu.com.
Miao YuKey Laboratory of Endocrinology, Ministry of Health, Translational Medical Center, Department of Endocrinology, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing 100730, China. yumiao_pumch@sohu.com.
Fan PingKey Laboratory of Endocrinology, Ministry of Health, Translational Medical Center, Department of Endocrinology, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing 100730, China. fanping_pumch@sohu.com.
Zhixin WangKey Laboratory of Endocrinology, Ministry of Health, Translational Medical Center, Department of Endocrinology, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing 100730, China. wangzhixinpumch@sohu.com.
Cuijuan QiKey Laboratory of Endocrinology, Ministry of Health, Translational Medical Center, Department of Endocrinology, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing 100730, China. qicuijuan_pumch@sohu.com.
Tong WangKey Laboratory of Endocrinology, Ministry of Health, Translational Medical Center, Department of Endocrinology, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing 100730, China. wangtong_pumch@sohu.com.
Xiaojing WangKey Laboratory of Endocrinology, Ministry of Health, Translational Medical Center, Department of Endocrinology, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing 100730, China. wangxiaojingpum@sohu.com.
Chinese Academy of Medical Sciences & Peking Union Medical College · CNPeking Union Medical College Hospital · CNQingdao University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It is now broadly accepted that the nutritional environment in early life is a key factor in susceptibility to metabolic diseases. In this study, we evaluated the effects of maternal chromium restriction in vivo on the modulation of lipid metabolism and the mechanisms involved in this process. Sixteen pregnant C57BL mice were randomly divided into two dietary treatments: a control (C) diet group and a low chromium (L) diet group. The diet treatment was maintained through gestation and lactation period. After weaning, some of the pups continued with either the control diet or low chromium diet (CC or LL), whereas other pups switched to another diet (CL or LC). At 32 weeks of age, serum lipid metabolism, proinflammatory indexes, oxidative stress and anti-oxidant markers, and DNA methylation status in adipose tissue were measured. The results indicated that the maternal low chromium diet increased body weight, fat pad weight, serum triglyceride (TG), low-density lipoprotein cholesterol (LDL), tumor necrosis factor-α (TNF-α), malondialdehyde (MDA), and oxidized glutathione (GSSG). There was a decrease in serum reduced/oxidized glutathione (GSH/GSSG) ratio at 32 weeks of age in female offspring. From adipose tissue, we identified 1214 individual hypomethylated CpG sites and 411 individual hypermethylated CpG sites in the LC group when compared to the CC group. Pathway analysis of the differential methylation genes revealed a significant increase in hypomethylated genes in the mitogen-activated protein kinase (MAPK) signaling pathway in the LC group. Our study highlights the importance of the MAPK signaling pathway in epigenetic changes involved in the lipid metabolism of the offspring from chromium-restricted dams.

Indexed as

Fetal DevelopmentLipid MetabolismMAP Kinase Signaling SystemMaternal Nutritional Physiological PhenomenaAdiposityAnimalsBiomarkersChromiumCpG IslandsDeficiency DiseasesDietary SupplementsDNA MethylationFemaleIntra-Abdominal FatLactationMice, Inbred C57BLBiomarkersChromiumchromium restriction dietDNA methylationlipid metabolismMAPK pathwaymetabolic programming

Identifiers

PMID27517955
PMCPMC4997401
OpenAlexW2493319833

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.