Evidence map›Paper›PMID 33830273›Full record

ArticleThe Journal of nutrition2021

Dietary Selenium Requirement for the Prevention of Glucose Intolerance and Insulin Resistance in Middle-Aged Mice.

Ying-Chen Huang, Tung-Lung Wu, Huawei Zeng, Wen-Hsing Cheng

Abstract read
In one paragraph

Article in The Journal of nutrition, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
–field-weighted citation impact
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

13 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Selenium status and type 2 diabetes risk.Archives of biochemistry and biophysics · 2022
    Review
  11. Article
  12. Article
  13. Review
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.

Ying-Chen HuangDepartment of Food Science, Nutrition, and Health Promotion, Mississippi State University, Mississippi State, MS, USA.
Tung-Lung WuDepartment of Mathematics and Statistics, Mississippi State University, Mississippi State, MS, USA.
Huawei ZengGrand Forks Human Nutrition Center, Agricultural Research Service, USDA, Grand Forks, ND, USA.
Wen-Hsing ChengDepartment of Food Science, Nutrition, and Health Promotion, Mississippi State University, Mississippi State, MS, USA.ORCID 0000-0003-2720-5164

Funding

Training and Mentoring Core P20GM103476 · NIGMS · UNIVERSITY OF SOUTHERN MISSISSIPPI · PI MICHAEL R GARRETT · 2012 to 2026
$60.2M
Optimized Selenium Intake, Gut Microbiota, and DiabetesR15DK117407 · NIDDK · MISSISSIPPI STATE UNIVERSITY · PI CHENG, WEN-HSING · 2018 to 2018
$421k
NIDDK NIH HHS R15 DK117407NIGMS NIH HHS P20 GM103476
6 · The paper itself

Abstract

backgroundAlthough dietary selenium (Se) deficiency or excess induces type 2 diabetes-like symptoms in mice, suboptimal body Se status usually causes no symptoms but may promote age-related decline in overall health.

objectivesWe sought to determine the dietary Se requirement for protection against type 2 diabetes-like symptoms in mice.

methodsThirty mature (aged 4 mo) male C57BL/6J mice were fed a Se-deficient torula yeast AIN-93M diet supplemented with Na2SeO4 in graded concentrations totaling 0.01 (basal), 0.04, 0.07, 0.10, and 0.13 (control) mg Se/kg for 4 mo (n = 6) until they were middle-aged (8 mo). Droplets of whole blood were used to determine glucose tolerance and insulin sensitivity in the mice from ages 5 to 8 mo. Postmortem serum, liver, and skeletal muscle were collected to assay for selenoprotein expression and markers of glucose metabolism. Data were analyzed by 1-way ANCOVA with or without random effects for time-repeated measurements using live mice or postmortem samples, respectively.

resultsCompared with control, the consumption of basal diet increased (P < 0.05) fasting serum insulin (95% CI: 52%, 182%) and leptin (95% CI: 103%, 118%) concentrations in middle-aged mice. Dietary Se insufficiency decreased (P < 0.05) 1) glucose tolerance (13-79%) and insulin sensitivity (15-65%) at ≤0.10 mg Se/kg; 2) baseline thymoma viral proto-oncogene phosphorylation on S473 (27-54%) and T308 (22-46%) at ≤0.10 and ≤0.07 mg Se/kg, respectively, in the muscle but not the liver; and 3) serum glutathione peroxidase 3 (51-83%), liver and muscle glutathione peroxidase 1 (32-84%), serum and liver selenoprotein P (28-42%), and liver and muscle selenoprotein H (39-48%) and selenoprotein W (16-73%) protein concentrations at ≤0.04, ≤0.10, ≤0.07, and ≤0.10 mg Se/kg, respectively.

conclusionsMice fed diets containing ≤0.10 mg Se/kg display impaired glucose tolerance and insulin sensitivity, suggesting increased susceptibility to type 2 diabetes by suboptimal Se status at levels ≤23% of nutritional needs.

Indexed as

Diabetes Mellitus, Type 2Glucose IntoleranceInsulin ResistanceSeleniumAnimalsMaleMiceMice, Inbred C57BLSeleniumageglucose intoleranceinsulin resistanceseleniumtype 2 diabetes

Identifiers

PMID33830273
PMCPMC8502482

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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.