Evidence map›Paper›PMID 34983495›Full record

ArticleBMC endocrine disorders2022

The role of CD36-Fabp4-PPARγ in skeletal muscle involves insulin resistance in intrauterine growth retardation mice with catch-up growth.

Jing Liu, Hang Zhao, Linlin Yang, Xing Wang, Linquan Yang, Yuling Xing, Xiuqin Lv, Huijuan Ma, Guangyao Song

Open access · goldAbstract read
In one paragraph

Article in BMC endocrine disorders, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
5.3field-weighted citation impact, top 5% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.

  1. Pooled it
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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

9 authors at 2 institutions in 1 country.

Jing LiuDepartment of Internal Medicine, Hebei Medical University, Shijiazhuang, 050017, Hebei, China.
Hang ZhaoDepartment of Endocrinology, Hebei General Hospital, Shijiazhuang, 050051, Hebei, China.
Linlin YangHebei Key Laboratory of Metabolic Diseases, Shijiazhuang, 050051, Hebei, China.
Xing WangHebei Key Laboratory of Metabolic Diseases, Shijiazhuang, 050051, Hebei, China.
Linquan YangHebei Key Laboratory of Metabolic Diseases, Shijiazhuang, 050051, Hebei, China.
Yuling XingDepartment of Internal Medicine, Hebei Medical University, Shijiazhuang, 050017, Hebei, China.
Xiuqin LvDepartment of Internal Medicine, Hebei Medical University, Shijiazhuang, 050017, Hebei, China.
Huijuan MaDepartment of Internal Medicine, Hebei Medical University, Shijiazhuang, 050017, Hebei, China. huijuanma76@163.com.
Guangyao SongDepartment of Internal Medicine, Hebei Medical University, Shijiazhuang, 050017, Hebei, China. sguangyao2@163.com.
Hebei General Hospital · CNHebei Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundStudies have shown that the high incidence of type 2 diabetes in China is associated with low birth weight and excessive nutrition in adulthood, which occurred during the famine years of the 1950s and 1960s, though the specific molecular mechanisms are unclear. In this study, we proposed a severe maternal caloric restriction during late pregnancy, followed by a post weaning high-fat diet in mice. After weaning, normal and high-fat diets were provided to mice to simulate the dietary pattern of modern society.

methodsThe pregnant mice were divided into two groups: normal birth weight (NBW) group and low birth weight (LBW) group. After 3 weeks for weaning, the male offspring mice in the NBW and LBW groups were then randomly divided into four subgroups: NC, NH, LC and LC groups. The offspring mice in the NC, NH, LC and LC groups were respectively fed with normal diet, normal diet, high-fat diet and high-fat diet for 18 weeks. After 18 weeks of dietary intervention, detailed analyses of mRNA and protein expression patterns, signaling pathway activities, and promoter methylation states were conducted for all relevant genes.

resultsAfter dietary intervention for 18 weeks, the expressions of CD36, Fabp4, PPARγ, FAS, and ACC1 in the skeletal muscle tissue of the LH group were significantly increased compared with the LC and NH groups (P < 0.05). The level of p-AMPK/AMPK in the skeletal muscle tissue of the LH group was significantly decreased compared with the LC and NH groups (P < 0.05). CPT1 and PGC-1α protein expressions were up-regulated in the LH group (P < 0.05) compared to the LC group. Additionally, the DNA methylation levels of the PGC-1α and GLUT4 gene promoters in the skeletal muscle of the LH groups were higher than those of the LC and NH groups (P < 0.05). However, PPARγ DNA methylation level in the LH group was lower than those of the LC and NH groups (P < 0.05).

conclusionsLBW combined with high-fat diets may increase insulin resistance and diabetes through regulating the CD36-related Fabp4-PPARγ and AMPK/ACC signaling pathways.

Indexed as

Diet, High-FatAnimalsCD36 AntigensDisease Models, AnimalFatty Acid-Binding ProteinsFemaleFetal Growth RetardationHumansInfant, Low Birth WeightInsulin ResistanceMaleMuscle, SkeletalPPAR gammaPregnancySignal TransductionCD36 AntigensFabp4 protein, mouseFatty Acid-Binding ProteinsPPAR gammaCD36Insulin resistanceLow birth weight

Identifiers

PMID34983495
PMCPMC8725347
OpenAlexW4206336089

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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.