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Cited by 105Nitric Oxide and Endothelin EffectsMetabolism, Diabetes, and CancerNatural Antidiabetic Agents Studies

The DOI matches its Crossref record; 46 of the 46 references it cites were found in a registry or an index.

Dietary nitrite improves insulin signaling through GLUT4 translocation

Jiang, Hong, Torregrossa, Ashley C., Potts, Amy, Pierini, Dan, Aranke, Mayank, Garg, Harsha K., Bryan, Nathan S.·2014·Free Radical Biology and Medicine
DOI 10.1016/j.freeradbiomed.2013.10.809
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Abstract

Diabetes mellitus type 2 is a syndrome of disordered metabolism with inappropriate hyperglycemia owing to a reduction in the biological effectiveness of insulin. Type 2 diabetes is associated with an impaired nitric oxide (NO) pathway that probably serves as the key link between metabolic disorders and cardiovascular disease. Insulin-mediated translocation of GLUT4 involves the PI3K/Akt kinase signal cascade that results in activation of endothelial NO synthase (eNOS). eNOS is dysfunctional during diabetes. We hypothesize that loss of eNOS-derived NO terminates the signaling cascade and therefore cannot activate GLUT4 translocation and that dietary nitrite may repair this pathway. In this study, we administered 50mg/L sodium nitrite to db/db diabetic mice for 4 weeks. After 4 weeks treatment, the db/db mice experienced less weight gain, improved fasting glucose levels, and reduced insulin levels. Cell culture experiments using CHO-HIRc-myc-GLUT4eGFP cell lines stably expressing insulin receptor and myc-GLUT4eGFP protein, as well as L6 skeletal muscle cells stably expressing rat GLUT4 with a Myc epitope (L6-GLUT4myc), showed that NO, nitrite, and GSNO stimulate GLUT4 translocation independent of insulin, which is inhibited by NEM. Collectively our data suggest that nitrite improves insulin signaling through restoration of NO-dependent nitrosation of GLUT4 signaling translocation. These data suggest that NO-mediated nitrosation of GLUT4 by nitrite or other nitrosating agents is necessary and sufficient for GLUT4 translocation in target tissue. Description of this pathway may justify a high-nitrate/nitrite diet along with the glycemic index to provide a safe and nutritional regimen for the management and treatment of diabetes.

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Metadata

Authors
Jiang, H., Torregrossa, A. C., Potts, A., Pierini, D., Aranke, M., Garg, H. K., & Bryan, N. S.
Affiliations
  • Brown Foundation Institute of Molecular Medicine for the Prevention of Human Diseases (US)
  • California State University, Fullerton (US)
  • The University of Texas at Austin (US)
Corresponding author
Bryan, Nathan S.
ORCID
Venue
Free Radical Biology and Medicine
Publisher
Elsevier BV
Published
2014-02
Volume
67
Pages
51-57
ISSN
0891-5849 (ISSN-L)
DOI
10.1016/j.freeradbiomed.2013.10.809
OpenAlex
W2049215298
Cited by
105
References
45
Citations by year
2026: 6 · 2025: 3 · 2024: 8 · 2023: 8 · 2022: 7 · 2021: 9 · 2020: 11 · 2019: 12 · 2018: 7 · 2017: 13 · 2016: 7 · 2015: 11 · 2014: 3
FWCI
4.86
Type
journal article
Language
en
Open access
closed
Licence
Locations
  • Free Radical Biology and Medicine (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • University of Texas Health Science Center at Houston
  • Hospital for Sick Children
Topics
  • Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Natural Antidiabetic Agents Studies
Keywords
dietary nitrite, sodium nitrite, insulin signaling, GLUT4 translocation, nitric oxide, type 2 diabetes, endothelial nitric oxide synthase, PI3K/Akt signaling, nitrosation, S-nitrosoglutathione, db/db mice, skeletal muscle, glycemic control
MeSH terms
Animals, Diabetes Mellitus, Type 2, Disease Models, Animal, Ethylmaleimide, Gene Expression Regulation, Humans, Male, Mice, Transgenic, Nitric Oxide, Receptor, Insulin, Sodium Nitrite, Signal Transduction, Proto-Oncogene Proteins c-myc, Protein Transport, Glucose Transporter Type 4, Mice, Rats, Nitric Oxide Synthase Type III

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