Evidence map›Paper›PMID 23372018›Full record

ArticleEndocrinology2013

Manganese supplementation protects against diet-induced diabetes in wild type mice by enhancing insulin secretion.

Soh-Hyun Lee, Hani A Jouihan, Robert C Cooksey, Deborah Jones, Hyung J Kim, Dennis R Winge, Donald A McClain

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 15% 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

47 citing papers in PubMed, 1 synthesis or guideline pooled it, 97 citations in OpenAlex.

  1. Pooled it
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  7. Article
  8. Cardiac oxidative damage and mitochondrial dysfunction induced by manganese deficiency are probably associated with the inhibition of the Nrf2 signaling pathway.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026
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  18. Frontiers in endocrinology · 2024
    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

7 authors at 1 institution in 1 country.

Soh-Hyun LeeDepartments of Internal Medicine and Biochemistry, Veterans Affairs Medical Center, Salt Lake City, UT 84132, USA.
Hani A Jouihan
Robert C Cooksey
Deborah Jones
Hyung J Kim
Dennis R Winge
Donald A McClain
University of Utah · US

Funding

UNIVERSITY OF UTAH CENTER FOR CLINICAL AND TRANSLATIONAL SCIENCE-UL1: BPCAUL1RR025764 · NCRR · UNIVERSITY OF UTAH · PI MCCLAIN, DONALD A. · 2008 to 2011
$19.4M
IRON AND METABOLISM: ALTERED FUEL OXIDATION AND MITOCHONDRIAL DYSFUNCTIONR01DK081842 · NIDDK · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI MCCLAIN, DONALD A. · 2009 to 2017
$3.9M
EXTRAMURAL RESEARCH FACILITIES CONSTRUCTIONC06RR011234 · NCRR · UNIVERSITY OF UTAH · PI MATSEN, JOHN M · 1995 to 1995
–
NCRR NIH HHS C06 RR011234NCRR NIH HHS UL1 RR025764NCRR NIH HHS UL1-RR025764NIDDK NIH HHS DK-081842NIDDK NIH HHS R01 DK081842
6 · The paper itself

Abstract

Mitochondrial dysfunction is both a contributing mechanism and complication of diabetes, and oxidative stress contributes to that dysfunction. Mitochondrial manganese-superoxide dismutase (MnSOD) is a metalloenzyme that provides antioxidant protection. We have previously shown in a mouse model of hereditary iron overload that cytosolic iron levels affected mitochondrial manganese availability, MnSOD activity, and insulin secretion. We therefore sought to determine the metallation status of MnSOD in wild-type mice and whether altering that status affected β-cell function. 129/SvEVTac mice given supplemental manganese exhibited a 73% increase in hepatic MnSOD activity and increased metallation of MnSOD. To determine whether manganese supplementation offered glucose homeostasis under a situation of β-cell stress, we challenged C57BL/6J mice, which are more susceptible to diet-induced diabetes, with a high-fat diet for 12 weeks. Manganese was supplemented or not for the final 8 weeks on that diet, after which we examined glucose tolerance and the function of isolated islets. Liver mitochondria from manganese-injected C57BL/6J mice had similar increases in MnSOD activity (81%) and metallation as were seen in 129/SvEVTac mice. The manganese-treated group fed high fat had improved glucose tolerance (24% decrease in fasting glucose and 41% decrease in area under the glucose curve), comparable with mice on normal chow and increased serum insulin levels. Isolated islets from the manganese-treated group exhibited improved insulin secretion, decreased lipid peroxidation, and improved mitochondrial function. In conclusion, MnSOD metallation and activity can be augmented with manganese supplementation in normal mice on normal chow, and manganese treatment can increase insulin secretion to improve glucose tolerance under conditions of dietary stress.

Indexed as

AnimalsDiabetes Mellitus, ExperimentalDietary SupplementsDiet, High-FatGlucose Tolerance TestInsulinInsulin-Secreting CellsInsulin SecretionLipid PeroxidationLiverMaleManganeseMiceMice, 129 StrainMice, Inbred C57BLOxidative StressInsulinManganeseSuperoxide Dismutase

Identifiers

PMID23372018
PMCPMC3578995
OpenAlexW1964548658

What OpenQuestion holds

Textmetadata
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.