Evidence map›Paper›PMID 26100787›Full record

ArticleEndocrine2016

Testosterone stimulates glucose uptake and GLUT4 translocation through LKB1/AMPK signaling in 3T3-L1 adipocytes.

Kazuteru Mitsuhashi, Takafumi Senmaru, Takuya Fukuda, Masahiro Yamazaki, Katsuhiko Shinomiya, Morio Ueno, Shigeru Kinoshita, Jo Kitawaki, Masato Katsuyama, Muneo Tsujikawa and 3 more

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In one paragraph

Article in Endocrine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

37 citing papers in PubMed, 55 citations in OpenAlex.

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  9. Effects of Fasting on Metabolic Hormones and Functions: A Narrative Review.Juntendo Iji zasshi = Juntendo medical journal · 2024
    Review
  10. Sexual Dimorphism in Cardiometabolic Diseases: The Role of AMPK.International journal of molecular sciences · 2023
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 1 institution in 1 country.

Kazuteru MitsuhashiDepartment of Endocrinology and Metabolism, Kyoto Prefectural University of Medicine, Graduate School of Medical Science, 465 Kajii-cho, Kawaramachi-Hirokoji, Kamigyo-ku, Kyoto, 602-8566, Japan.
Takafumi SenmaruDepartment of Endocrinology and Metabolism, Kyoto Prefectural University of Medicine, Graduate School of Medical Science, 465 Kajii-cho, Kawaramachi-Hirokoji, Kamigyo-ku, Kyoto, 602-8566, Japan. semmarut@koto.kpu-m.ac.jp.
Takuya FukudaDepartment of Endocrinology and Metabolism, Kyoto Prefectural University of Medicine, Graduate School of Medical Science, 465 Kajii-cho, Kawaramachi-Hirokoji, Kamigyo-ku, Kyoto, 602-8566, Japan.
Masahiro YamazakiDepartment of Endocrinology and Metabolism, Kyoto Prefectural University of Medicine, Graduate School of Medical Science, 465 Kajii-cho, Kawaramachi-Hirokoji, Kamigyo-ku, Kyoto, 602-8566, Japan.
Katsuhiko ShinomiyaDepartment of Ophthalmology, Kyoto Prefectural University of Medicine, Graduate School of Medical Science, Kyoto, Japan.
Morio UenoDepartment of Ophthalmology, Kyoto Prefectural University of Medicine, Graduate School of Medical Science, Kyoto, Japan.
Shigeru KinoshitaDepartment of Ophthalmology, Kyoto Prefectural University of Medicine, Graduate School of Medical Science, Kyoto, Japan.
Jo KitawakiDepartment of Obstetrics and Gynecology, Kyoto Prefectural University of Medicine, Graduate School of Medical Science, Kyoto, Japan.
Masato KatsuyamaRadioisotope Center, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Muneo TsujikawaInstitute of Bio-Response Informatics, Kyoto, Japan.
Hiroshi ObayashiInstitute of Bio-Response Informatics, Kyoto, Japan.
Naoto NakamuraDepartment of Endocrinology and Metabolism, Kyoto Prefectural University of Medicine, Graduate School of Medical Science, 465 Kajii-cho, Kawaramachi-Hirokoji, Kamigyo-ku, Kyoto, 602-8566, Japan.
Michiaki FukuiDepartment of Endocrinology and Metabolism, Kyoto Prefectural University of Medicine, Graduate School of Medical Science, 465 Kajii-cho, Kawaramachi-Hirokoji, Kamigyo-ku, Kyoto, 602-8566, Japan.
Kyoto Prefectural University of Medicine · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Decreases in serum testosterone concentrations in aging men are associated with metabolic disorders. Testosterone has been reported to increase GLUT4-dependent glucose uptake in skeletal muscle cells and cardiomyocytes. However, studies on glucose uptake occurring in response to testosterone stimulation in adipocytes are currently not available. This study was designed to determine the effects of testosterone on glucose uptake in adipocytes. Glucose uptake was assessed with 2-[(3)H] deoxyglucose in 3T3-L1 adipocytes. GLUT4 translocation was evaluated in plasma membrane (PM) sheets and PM fractions by immunofluorescence and immunoblotting, respectively. Activation of GLUT4 translocation-related protein kinases, including Akt, AMPK, LKB1, CaMKI, CaMKII, and Cbl was followed by immunoblotting. Expression levels of androgen receptor (AR) mRNA and AR translocation to the PM were assessed by real-time RT-PCR and immunoblotting, respectively. The results showed that both high-dose (100 nM) testosterone and testosterone-BSA increased glucose uptake and GLUT4 translocation to the PM, independently of the intracellular AR. Testosterone and testosterone-BSA stimulated the phosphorylation of AMPK, LKB1, and CaMKII. The knockdown of LKB1 by siRNA attenuated testosterone- and testosterone-BSA-stimulated AMPK phosphorylation and glucose uptake. These results indicate that high-dose testosterone and testosterone-BSA increase GLUT4-dependent glucose uptake in 3T3-L1 adipocytes by inducing the LKB1/AMPK signaling pathway.

Indexed as

3T3-L1 CellsAdipocytesAMP-Activated Protein KinasesAnimalsCarbohydrate MetabolismGlucoseGlucose Transporter Type 4MicePhosphorylationProtein Serine-Threonine KinasesProtein TransportSignal TransductionTestosteroneAMP-Activated Protein KinasesGlucoseGlucose Transporter Type 4Protein Serine-Threonine KinasesStk11 protein, mouseTestosteroneAMPK signalingGlucose uptakeGLUT4 translocationNon-genomic actionTestosterone

Identifiers

PMID26100787
OpenAlexW4232953156

What OpenQuestion holds

Textmetadata
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.