Evidence map›Paper›PMID 29373583›Full record

ArticlePloS one2018

Zinc stimulates glucose oxidation and glycemic control by modulating the insulin signaling pathway in human and mouse skeletal muscle cell lines.

Shaghayegh Norouzi, John Adulcikas, Sukhwinder Singh Sohal, Stephen Myers

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 1 pooled it
4.8field-weighted citation impact, top 4% 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

46 citing papers in PubMed, 1 synthesis or guideline pooled it, 87 citations in OpenAlex.

  1. Pooled it
  2. Trial
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  11. Vanadium Compound Treatment Modulates MC3t3-E1 Osteoblast Function.International journal of molecular sciences · 2025
    Article
  12. Zinc Alleviates Gut Barrier Dysfunction by Promoting the Methylation of AKT.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  13. Review
  14. Evaluation of lipid profile, liver function enzymes, and trace elements in Iraqi diabetic nephropathy patients.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2024
    Article
  15. Article
  16. Review
  17. Circulating zinc levels and cardiometabolic risk-related variables in adultsBiomedica : revista del Instituto Nacional de Salud · 2024
    Article
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  19. Article
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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

4 authors at 1 institution in 1 country.

Shaghayegh NorouziCollege of Health and Medicine, School of Health Sciences, University of Tasmania, Newnham Campus, Launceston, Tasmania, Australia.
John AdulcikasCollege of Health and Medicine, School of Health Sciences, University of Tasmania, Newnham Campus, Launceston, Tasmania, Australia.
Sukhwinder Singh SohalCollege of Health and Medicine, School of Health Sciences, University of Tasmania, Newnham Campus, Launceston, Tasmania, Australia.
Stephen MyersCollege of Health and Medicine, School of Health Sciences, University of Tasmania, Newnham Campus, Launceston, Tasmania, Australia.ORCID 0000-0003-4793-3820
University of Tasmania · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Zinc is a metal ion that is an essential cell signaling molecule. Highlighting this, zinc is an insulin mimetic, activating cellular pathways that regulate cellular homeostasis and physiological responses. Previous studies have linked dysfunctional zinc signaling with several disease states including cancer, obesity, cardiovascular disease and type 2 diabetes. The present study evaluated the insulin-like effects of zinc on cell signaling molecules including tyrosine, PRSA40, Akt, ERK1/2, SHP-2, GSK-3β and p38, and glucose oxidation in human and mouse skeletal muscle cells. Insulin and zinc independently led to the phosphorylation of these proteins over a 60-minute time course in both mouse and human skeletal muscle cells. Similarly, utilizing a protein array we identified that zinc could active the phosphorylation of p38, ERK1/2 and GSK-3B in human and ERK1/2 and GSK-3B in mouse skeletal muscle cells. Glucose oxidation assays were performed on skeletal muscle cells treated with insulin, zinc, or a combination of both and resulted in a significant induction of glucose consumption in mouse (p<0.01) and human (p<0.05) skeletal muscle cells when treated with zinc alone. Insulin, as expected, increased glucose oxidation in mouse (p<0.001) and human (0.001) skeletal muscle cells, however the combination of zinc and insulin did not augment glucose consumption in these cells. Zinc acts as an insulin mimetic, activating key molecules implicated in cell signaling to maintain glucose homeostasis in mouse and human skeletal muscle cells. Zinc is an important metal ion implicated in several biological processes. The role of zinc as an insulin memetic in activating key signaling molecules involved in glucose homeostasis could provide opportunities to utilize this ion therapeutically in treating disorders associated with dysfunctional zinc signaling.

Indexed as

AnimalsBlood GlucoseCell LineGlucoseHumansInsulinMiceMuscle, SkeletalOxidation-ReductionSignal TransductionZincBlood GlucoseGlucoseInsulinZinc

Identifiers

PMID29373583
PMCPMC5786307
OpenAlexW2785156213

What Socratic holds

Textmetadata
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 Socratic graph.