Evidence map›Paper›PMID 31071176›Full record

ArticlePloS one2019

Reduction of the PI3K/Akt related signaling activities in skeletal muscle tissues involves insulin resistance in intrauterine growth restriction rats with catch-up growth.

Yan Xing, Jin Zhang, Hongling Wei, Hui Zhang, Yuhong Guan, Xinli Wang, Xiaomei Tong

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
8.0field-weighted citation impact, top 3% 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

25 citing papers in PubMed, 32 citations in OpenAlex.

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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

7 authors at 2 institutions in 1 country.

Yan XingDepartment of Pediatrics, Peking University Third Hospital, Beijing, China.
Jin ZhangDepartment of pediatrics, Beijing Jishuitan Hospital, Beijing, China.
Hongling WeiDepartment of Pediatrics, Peking University Third Hospital, Beijing, China.
Hui ZhangDepartment of Pediatrics, Peking University Third Hospital, Beijing, China.
Yuhong GuanDepartment of Pulmonary, Beijing Children's Hospital, Capital Medical University, Beijing, China.
Xinli WangDepartment of Pediatrics, Peking University Third Hospital, Beijing, China.ORCID 0000-0001-5990-4117
Xiaomei TongDepartment of Pediatrics, Peking University Third Hospital, Beijing, China.
Peking University · CNCapital Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Individuals with intrauterine growth retardation (IUGR) are prone to insulin resistance, whereas the underlying molecular mechanisms remain unclear. In this study, we investigated if the PI3K/Akt signaling pathway in skeletal muscle tissues involves insulin resistance in IUGR offsprings, particularly ones with catch-up growth. An IUGR rat model was established by feeding rats an isocaloric (30.50 Kcal/g) diet containing 8% protein (low-protein diet) from day 1 of pregnancy until the birth of their pups. Glucometabolic parameters were measured and compared. Quantitative PCR and western blot were performed to assess mRNA and protein expression changes of the PI3K/Akt related signals in skeletal muscle tissues. Pearson analysis was used to assess the correlation of the PI3K/Akt signaling level and catch-up growth with the insulin resistance index (IRI). The values of fasting plasma glucose, fasting insulin and IRI were significantly higher, whereas insulin sensitivity index was significantly lower in IUGR offsprings than those in the controls. The PI3K mRNA and protein levels as well as the phospho-AktSer473 levels were significantly lower in IUGR offsprings compared to the controls. Reductions of GLUT4 as well as increases of PTEN and nuclear fractional PPARγ were detected in IUGR offsprings. Catch-up growth IUGR rats were positively correlated with insulin resistance and underwent more remarkable alterations of the PI3K, PTEN and GLUT4 expressions. Our results demonstrated that rats born IUGR developed insulin resistance later in life, which was likely mediated by reductions of the PI3K/Akt related signaling activities, particularly in those with excess catch-up growth.

Indexed as

AnimalsAnimals, NewbornDisease Models, AnimalFemaleFetal Growth RetardationGlucose Transporter Type 4Insulin ResistanceMuscle, SkeletalPhosphatidylinositol 3-KinasesPPAR gammaPregnancyProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseRatsRats, Sprague-DawleyRNA, MessengerGlucose Transporter Type 4Phosphatidylinositol 3-KinasesPPAR gammaProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePten protein, ratRNA, MessengerSlc2a4 protein, rat

Identifiers

PMID31071176
PMCPMC6508867
OpenAlexW2944511835

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.