Evidence map›Paper›PMID 33420419›Full record

ArticleCommunications biology2021

AdipoR agonist increases insulin sensitivity and exercise endurance in AdipoR-humanized mice.

Masato Iwabu, Miki Okada-Iwabu, Hiroaki Tanabe, Nozomi Ohuchi, Keiko Miyata, Toshiko Kobori, Sara Odawara, Yuri Kadowaki, Shigeyuki Yokoyama, Toshimasa Yamauchi and 1 more

Abstract read
In one paragraph

Article in Communications biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
–field-weighted citation impact
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

19 citing papers in PubMed.

  1. Exercise pills for cardiometabolic health cannot mimic the exercise milieu.Trends in endocrinology and metabolism: TEM · 2026
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  12. Molecular origin and biological effects of exercise mimetics.Journal of exercise science and fitness · 2024
    Review
  13. Article
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  15. Article
  16. Article
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  18. Vascular endothelial adiponectin signaling across the life span.American journal of physiology. Heart and circulatory physiology · 2022
    Review
  19. Review
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.

Masato IwabuDepartment of Diabetes and Metabolic Diseases, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-0033, Japan.
Miki Okada-IwabuDepartment of Diabetes and Metabolic Diseases, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-0033, Japan. omiki-tky@umin.ac.jp.ORCID 0000-0002-5099-2760
Hiroaki TanabeRIKEN Structural Biology Laboratory, 1-7-22 Suehiro-cho, Tsurumi-ku, Yokohama, 230-0045, Japan.ORCID 0000-0003-2424-9460
Nozomi OhuchiDepartment of Diabetes and Metabolic Diseases, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-0033, Japan.
Keiko MiyataDepartment of Diabetes and Metabolic Diseases, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-0033, Japan.
Toshiko KoboriDivision of Diabetes and Metabolism, The Institute for Adult Diseases, Asahi Life Foundation, 2-2-6 Nihonbashibakuro-cho, Chuo-ku, Tokyo, 103-0002, Japan.
Sara OdawaraDepartment of Diabetes and Metabolic Diseases, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-0033, Japan.
Yuri KadowakiDepartment of Diabetes and Metabolic Diseases, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-0033, Japan.
Shigeyuki YokoyamaRIKEN Structural Biology Laboratory, 1-7-22 Suehiro-cho, Tsurumi-ku, Yokohama, 230-0045, Japan.ORCID 0000-0003-3133-7338
Toshimasa YamauchiDepartment of Diabetes and Metabolic Diseases, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-0033, Japan. tyamau-tky@umin.ac.jp.ORCID 0000-0003-4827-6404
Takashi KadowakiDepartment of Diabetes and Metabolic Diseases, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-0033, Japan. t-kadowaki@toranomon.kkr.or.jp.ORCID 0000-0002-5428-3582

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Adiponectin receptors, AdipoR1 and AdipoR2 exert anti-diabetic effects. Although muscle-specific disruption of AdipoR1 has been shown to result in decreased insulin sensitivity and decreased exercise endurance, it remains to be determined whether upregulation of AdipoR1 could reverse them in obese diabetic mice. Here, we show that muscle-specific expression of human AdipoR1 increased expression levels of genes involved in mitochondrial biogenesis and oxidative stress-detoxification to almost the same extents as treadmill exercise, and concomitantly increased insulin sensitivity and exercise endurance in obese diabetic mice. Moreover, we created AdipoR-humanized mice which express human AdipoR1 in muscle of AdipoR1·R2 double-knockout mice. Most importantly, the small-molecule AdipoR agonist AdipoRon could exert its beneficial effects in muscle via human AdipoR, and increased insulin sensitivity and exercise endurance in AdipoR-humanized mice. This study suggests that expression of human AdipoR1 in skeletal muscle could be exercise-mimetics, and that AdipoRon could exert its beneficial effects via human AdipoR1.

Indexed as

Insulin ResistanceAnimalsDrug Evaluation, PreclinicalExercise ToleranceMaleMiceMice, KnockoutObesityPiperidinesReceptors, AdiponectinADIPOR1 protein, humanAdipoRonPiperidinesReceptors, Adiponectin

Identifiers

PMID33420419
PMCPMC7794315

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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.