Evidence map›Paper›PMID 15897298›Full record

ReviewEndocrine reviews2005

Adiponectin and adiponectin receptors.

Takashi Kadowaki, Toshimasa Yamauchi

Registry-linked trialOpen access · bronzeAbstract readReview
PubMed Publisher
In one paragraph

Review in Endocrine reviews, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT01524705 (FLAT-SUGAR), which is not on this map. Cited by 863 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
863citing papers in PubMed, 6 pooled it
93.5field-weighted citation impact, top 1% 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.

NCT01524705 phase4completedstarted 2012, after this paper: background citation

FLAT-SUGAR: FLuctuATion Reduction With inSULin and Glp-1 Added togetheR

Ran2012Enrolled102Registered outcomes4Posted comparisons3ConditionsType 2 DiabetesArmsexenatide, Insulin glargine, Metformin, Prandial insulin
PMID 19092145PMID 27208320PMID 11466120PMID 15251625PMID 15326314PMID 15857227PMID 15939816PMID 12765959PMID 12716809PMID 12711737PMID 11916939PMID 11865066other papers from this trial
Open the trial in the graph
3 · Its place in the literature

Who cites it

863 citing papers in PubMed, 6 syntheses or guidelines pooled it, 2,592 citations in OpenAlex.

  1. Pooled it
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  5. A Systematic Narrative Review onEndocrine, metabolic & immune disorders drug targets · 2024
    Pooled it
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  10. Safety and Effects ofNutrients · 2023
    Trial
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  17. Investigating the Role ofJournal of clinical research in pediatric endocrinology · 2026
    Article
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  20. Article

803 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Takashi KadowakiDepartment of Metabolic Diseases, Graduate School of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan. kadowaki-3im@h.u-tokyo.ac.jp
Toshimasa Yamauchi
Japan Science and Technology Agency · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metabolic syndrome is thought to result from obesity and obesity-linked insulin resistance. Obesity in adulthood is characterized by adipocyte hypertrophy. Adipose tissue participates in the regulation of energy homeostasis as an important endocrine organ that secretes a number of biologically active "adipokines."Heterozygous peroxisome proliferator-activated receptor-gamma knockout mice were protected from high-fat diet induced obesity, adipocyte hypertrophy, and insulin resistance. Systematic gene profiling analysis of these mice revealed that adiponectin/Acrp30 was overexpressed. Functional analyses including generation of adiponectin transgenic or knockout mice have revealed that adiponectin serves as an insulin-sensitizing adipokine. In fact, obesity-linked down-regulation of adiponectin was a mechanism whereby obesity could cause insulin resistance and diabetes. Recently, we have cloned adiponectin receptors in the skeletal muscle (AdipoR1) and liver (AdipoR2), which appear to comprise a novel cell-surface receptor family. We showed that AdipoR1 and AdipoR2 serve as receptors for globular and full-length adiponectin and mediate increased AMP-activated protein kinase, peroxisome proliferator-activated receptor-alpha ligand activities, and glucose uptake and fatty-acid oxidation by adiponectin. Obesity decreased expression levels of AdipoR1/R2, thereby reducing adiponectin sensitivity, which finally leads to insulin resistance, the so-called "vicious cycle." Most recently, we showed that osmotin, which is a ligand for the yeast homolog of AdipoR (PHO36), activated AMPK via AdipoR in C2C12 myocytes. This may facilitate efficient development of adiponectin receptor agonists. Adiponectin receptor agonists and adiponectin sensitizers should serve as versatile treatment strategies for obesity-linked diseases such as diabetes and metabolic syndrome.

Indexed as

AdiponectinAnimalsArteriosclerosisDisease Models, AnimalHumansInsulin ResistanceIntercellular Signaling Peptides and ProteinsLiverMetabolic SyndromeMiceModels, MolecularMuscle, SkeletalReceptors, AdiponectinReceptors, Cell SurfaceAdiponectinadiponectin receptor 1, mouseadiponectin receptor 2, mouseIntercellular Signaling Peptides and ProteinsReceptors, AdiponectinReceptors, Cell Surface

Identifiers

PMID15897298
OpenAlexW1971452427

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.