Evidence map›Paper›PMID 31270755›Full record

ArticleMolecular biology reports2019

Endogenous SHBG levels correlate with that of glucose transporters in insulin resistance model cells.

Chong Feng, Zhen Jin, Lei Sun, Xiaoyan Wang, Xinshu Chi, Xuan Zhang, Siyu Lian

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular biology reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

16 citing papers in PubMed, 18 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 1 institution in 1 country.

Chong FengDepartment of Obstetrics and Gynecology, Shengjing Hospital Affiliated to China Medical University, No. 36, Sanhao Street, Heping District, Shenyang, 110004, China.ORCID http://orcid.org/0000-0003-4298-715X
Zhen JinDepartment of Obstetrics and Gynecology, Shengjing Hospital Affiliated to China Medical University, No. 36, Sanhao Street, Heping District, Shenyang, 110004, China. JINZ_sjhospital@yahoo.com.ORCID http://orcid.org/0000-0003-2189-4069
Lei SunDepartment of Obstetrics and Gynecology, Shengjing Hospital Affiliated to China Medical University, No. 36, Sanhao Street, Heping District, Shenyang, 110004, China.ORCID http://orcid.org/0000-0001-5448-7406
Xiaoyan WangDepartment of Obstetrics and Gynecology, Shengjing Hospital Affiliated to China Medical University, No. 36, Sanhao Street, Heping District, Shenyang, 110004, China.ORCID http://orcid.org/0000-0001-7602-9107
Xinshu ChiDepartment of Obstetrics and Gynecology, Shengjing Hospital Affiliated to China Medical University, No. 36, Sanhao Street, Heping District, Shenyang, 110004, China.ORCID http://orcid.org/0000-0003-0225-7654
Xuan ZhangDepartment of Obstetrics and Gynecology, Shengjing Hospital Affiliated to China Medical University, No. 36, Sanhao Street, Heping District, Shenyang, 110004, China.ORCID http://orcid.org/0000-0002-3359-7283
Siyu LianDepartment of Obstetrics and Gynecology, Shengjing Hospital Affiliated to China Medical University, No. 36, Sanhao Street, Heping District, Shenyang, 110004, China.ORCID http://orcid.org/0000-0003-2093-2254
China Medical University · CN

Funding

National Natural Science Foundation of China 81170591National Natural Science Foundation of China 81300511
6 · The paper itself

Abstract

Gestational diabetes mellitus (GDM) is defined as glucose intolerance of any degree that occurs after onset of pregnancy. Sex hormone binding globulin (SHBG) plays an important regulatory role in insulin resistance and is a risk factor in GDM. In the current study, we aimed to examine whether SHBG can regulate glucose metabolism through glucose transporters (GLUTs). SHBG was transfected into established human insulin model cells and the expression of SHBG, GLUT1, GLUT3, and GLUT4 was detected and analyzed in normal cells, model cells, and all groups of transfected cells by real-time PCR and western blotting. Further, immunofluorescence staining was performed on cells from each group to observe protein expression. In insulin resistance model cells, the expression of SHBG was low, whereas that of GLUT1 was high and of GLUT3 and GLUT4 was low, when compared with expression in control cells. Moreover, the overexpression of SHBG inhibited the expression of GLUT1 mRNA and protein, and promoted the expression of GLUT3 and GLUT4. Our results indicate that SHBG could be involved in glucose metabolism through its regulation of multiple GLUTs. Transfection of SHBG into insulin-resistant cells may partially improve the level of GLUTs, providing a potential therapeutic approach for the treatment of insulin resistance in GDM. Although SHBG can regulate glucose metabolism through GLUTs and thus cause insulin resistance and induce gestational diabetes, the regulation mechanism of GLUTs mediated by SHBG has not been elucidated, which will be the focus of further studies.

Indexed as

Cell LineGlucose IntoleranceGlucose Transporter Type 1Glucose Transporter Type 3Glucose Transporter Type 4Glucose Transport Proteins, FacilitativeHumansInsulinInsulin ResistanceModels, BiologicalSex Hormone-Binding GlobulinTranscriptomeGlucose Transporter Type 1Glucose Transporter Type 3Glucose Transporter Type 4Glucose Transport Proteins, FacilitativeInsulinSex Hormone-Binding GlobulinSHBG protein, humanGestational diabetes mellitus (GDM)Glucose transporters (GLUTs)GLUT4 translocationHTR8/SVneoInsulin resistanceSex hormone binding globulin (SHBG)

Identifiers

PMID31270755
OpenAlexW2954959713

What OpenQuestion holds

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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.