Evidence map›Paper›PMID 24296248›Full record

ArticleFree radical biology & medicine2014

Renal improvement by zinc in diabetic mice is associated with glucose metabolism signaling mediated by metallothionein and Akt, but not Akt2.

Weixia Sun, Yuehui Wang, Xiao Miao, Yonggang Wang, Li Zhang, Ying Xin, Shirong Zheng, Paul N Epstein, Yaowen Fu, Lu Cai

Open access · greenAbstract read
In one paragraph

Article in Free radical biology & medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.5field-weighted citation impact, top 8% 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

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3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 49 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

10 authors at 6 institutions in 2 countries.

Weixia SunFirst Hospital, Jilin University, Jilin 130021, China; Kosair Children's Hospital Research Institute, Department of Pediatrics, University of Louisville, KY 40202, USA.
Yuehui WangSecond Hospital, Jilin University, Jilin 130041, China.
Xiao MiaoKosair Children's Hospital Research Institute, Department of Pediatrics, University of Louisville, KY 40202, USA; Second Hospital, Jilin University, Jilin 130041, China.
Yonggang WangKosair Children's Hospital Research Institute, Department of Pediatrics, University of Louisville, KY 40202, USA; China-Japan Union Hospital, Jilin University, Jilin 130031, China.
Li ZhangFirst Hospital, Jilin University, Jilin 130021, China.
Ying XinKosair Children's Hospital Research Institute, Department of Pediatrics, University of Louisville, KY 40202, USA; Norman Bethune Medical College, Jilin University, Jilin 130021, China.
Shirong ZhengKosair Children's Hospital Research Institute, Department of Pediatrics, University of Louisville, KY 40202, USA.
Paul N EpsteinKosair Children's Hospital Research Institute, Department of Pediatrics, University of Louisville, KY 40202, USA; Department of Pharmacology and Toxicology, University of Louisville, KY 40202, USA.
Yaowen FuFirst Hospital, Jilin University, Jilin 130021, China. Electronic address: fuyaowen@medmail.com.cn.
Lu CaiKosair Children's Hospital Research Institute, Department of Pediatrics, University of Louisville, KY 40202, USA; Department of Pharmacology and Toxicology, University of Louisville, KY 40202, USA. Electronic address: L0cai001@louisville.edu.
First Hospital of Jilin University · CNKosair Children's Hospital · USUniversity of Louisville · USFirst Bethune Hospital of Jilin University · CNSecond Affiliated Hospital of Jilin University · CNUnion Hospital · CN

Funding

Metabolomics study on the preventive mechanisms for LDR on diabetic nephropathyR01DK091338 · NIDDK · UNIVERSITY OF LOUISVILLE · PI CAI, LU · 2013 to 2014
$900k
NIDDK NIH HHS 1R01DK091338-01A1NIDDK NIH HHS R01 DK091338
6 · The paper itself

Abstract

Human epidemiological and animal studies have shown the beneficial effect of zinc supplementation on mitigating diabetic nephropathy. However, the mechanism by which zinc protects the kidney from diabetes remains unknown. Here we demonstrate the therapeutic effects of zinc on diabetes-induced renal pathological and functional changes. These abnormalities were found in both transgenic OVE26 and Akt2-KO diabetic mouse models, accompanied by significant changes in glucose-metabolism-related regulators. The changes included significantly decreased phosphorylation of Akt and GSK-3β, increased phosphorylation of renal glycogen synthase, decreased expression of hexokinase II and PGC-1α, and increased expression of the Akt negative regulators PTEN, PTP1B, and TRB3. All of these were significantly prevented by zinc treatment for 3 months. Furthermore, zinc-stimulated changes in glucose metabolism mediated by Akt were actually found to be metallothionein dependent, but not Akt2 dependent. These results suggest that the therapeutic effects of zinc in diabetic nephropathy are mediated, in part, by the preservation of glucose-metabolism-related pathways via the prevention of diabetes-induced upregulation of Akt negative regulators. Given that zinc deficiency is very common in diabetics, this finding implies that regularly monitoring zinc levels in diabetic patients, as well as supplementing if low, is important in mitigating the development of diabetic nephropathy.

Indexed as

AnimalsDiabetic NephropathiesDisease Models, AnimalGlucoseGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHumansMetallothioneinMiceMice, Inbred NODMice, TransgenicProto-Oncogene Proteins c-aktSignal TransductionZincAKT2 protein, humanGlucoseGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGSK3B protein, humanGsk3b protein, mouseMetallothioneinProto-Oncogene Proteins c-aktZincAkt, GSK-3β, Akt2 gene defectDiabetic nephropathyFree radicalsMetallothioneinZinc

Identifiers

PMID24296248
PMCPMC5288838
OpenAlexW2015511959

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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.