Evidence map›Paper›PMID 32835596›Full record

ArticleAdipocyte2020

The diabetes medication canagliflozin promotes mitochondrial remodelling of adipocyte via the AMPK-Sirt1-Pgc-1α signalling pathway.

Xuping Yang, Qinhui Liu, Yanping Li, Qin Tang, Tong Wu, Lei Chen, Shiyun Pu, Yingnan Zhao, Guorong Zhang, Cuiyuan Huang and 8 more

Open access · goldAbstract read
In one paragraph

Article in Adipocyte, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
104citing papers in PubMed, 1 pooled it
11.1field-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.

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

104 citing papers in PubMed, 1 synthesis or guideline pooled it, 166 citations in OpenAlex.

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  14. The D826V point mutation inFrontiers in cell and developmental biology · 2026
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44 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

18 authors at 6 institutions in 1 country.

Xuping YangDepartment of Pharmacy, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University . Chengdu China.
Qinhui LiuLaboratory of Clinical Pharmacy and Adverse Drug Reaction, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University , Chengdu China.
Yanping LiLaboratory of Clinical Pharmacy and Adverse Drug Reaction, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University , Chengdu China.
Qin TangDepartment of Pharmacy, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University . Chengdu China.
Tong WuDepartment of Pharmacy, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University . Chengdu China.
Lei ChenDepartment of Pharmacy, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University . Chengdu China.
Shiyun PuDepartment of Pharmacy, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University . Chengdu China.
Yingnan ZhaoDepartment of Pharmacy, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University . Chengdu China.
Guorong ZhangDepartment of Pharmacy, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University . Chengdu China.
Cuiyuan HuangDepartment of Pharmacy, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University . Chengdu China.
Jinhang ZhangDepartment of Pharmacy, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University . Chengdu China.
Zijing ZhangDepartment of Pharmacy, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University . Chengdu China.
Ya HuangDepartment of Pharmacy, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University . Chengdu China.
Min ZouDepartment of Pharmacy, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University . Chengdu China.
Xiongjie ShiCollege of Life Sciences, the Institute for Advanced Studies, Wuhan University , Wuhan, China.
Wei JiangMolecular Medicine Research Center, West China Hospital of Sichuan University , Chengdu, China.
Rui WangDepartment of Cardiology, Yangpu Hospital, Tongji University , Shanghai, China.
Jinhan HeDepartment of Pharmacy, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University . Chengdu China.
State Key Laboratory of BiotherapySichuan University · CNAffiliated Hospital of Southwest Medical University · CNWest China Hospital of Sichuan University · CNWuhan University · CNYangpu Hospital of Tongji University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The diabetes medication canagliflozin (Cana) is a sodium glucose cotransporter 2 (SGLT2) inhibitor acting by increasing urinary glucose excretion and thus reducing hyperglycaemia. Cana treatment also reduces body weight. However, it remains unclear whether Cana could directly work on adipose tissue. In the present study, the pharmacological effects of Cana and the associated mechanism were investigated in adipocytes and mice. Stromal-vascular fractions (SVFs) were isolated from subcutaneous adipose tissue and differentiated into mature adipocytes. Our results show that Cana treatment directly increased cellular energy expenditure of adipocytes by inducing mitochondrial biogenesis independently of SGLT2 inhibition. Along with mitochondrial biogenesis, Cana also increased mitochondrial oxidative phosphorylation, fatty acid oxidation and thermogenesis. Mechanistically, Cana promoted mitochondrial biogenesis and function via an Adenosine monophosphate-activated protein kinase (AMPK) - silent information regulator 1 (Sirt1) - peroxisome proliferator-activated receptor γ coactivator-1α (Pgc-1α) signalling pathway. Consistently, ABBREVIATIONS: Ucp-1, uncoupling protein 1; cAMP, cyclic adenosine monophosphate; PKA, cAMP-dependent protein kinase A; SGLT, sodium glucose cotransporter; Cana, canagliflozin; T2DM: type 2 diabetes; Veh, vehicle; Pgc-1α, peroxisome proliferator-activated receptor γ coactivator-1α; SVFs, stromal-vascular fractions; FBS, bovine serum; Ad, adenovirus; mtDNA, mitochondrial DNA; COX2, cytochrome oxidase subunit 2; RT-PCR, real-time PCR; SDS-PAGE, sodium dodecyl sulphate-polyacrylamide gel electrophoresis; Prdm16, PR domain zinc finger protein 16; Cidea, cell death inducing DFFA-like effector A; Pgc-1β, peroxisome proliferator-activated receptor γ coactivator-1β; NRF1, nuclear respiratory factor 1; Tfam, mitochondrial transcription factor A; OXPHOS, oxidative phosphorylation; FAO, fatty acid oxidation; AMPK, Adenosine monophosphate-activated protein kinase; p-AMPK, phosphorylated AMPK; Sirt1, silent information regulator 1; mTOR, mammalian target of rapamycin; WAT, white adipose tissue; Fabp4, fatty acid binding protein 4; Lpl, lipoprotein lipase; Slc5a2, solute carrier family 5 member 2; ERRα, oestrogen related receptor α; Uqcrc2, ubiquinol-cytochrome c reductase core protein 2; Uqcrfs1, ubiquinol-cytochrome c reductase, Rieske iron-sulphur polypeptide 1; Cox4, cytochrome c oxidase subunit 4; Pparα, peroxisome proliferator activated receptor α; NAD

Indexed as

AdipocytesAMP-Activated Protein KinasesAnimalsCanagliflozinEnergy MetabolismFatty AcidsGene Expression RegulationMaleMiceMitochondriaModels, BiologicalOrganelle BiogenesisOxidation-ReductionOxidative PhosphorylationPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaSignal TransductionAMP-Activated Protein KinasesCanagliflozinFatty AcidsPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPpargc1a protein, mouseSirtuin 1adipocytesCanagliflozinenergy homoeostasismitochondrial biogenesisPgc-1α

Identifiers

PMID32835596
PMCPMC7469612
OpenAlexW3081001956

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.