ArticleThe Journal of biological chemistry2020
Low-dose naltrexone rescues inflammation and insulin resistance associated with hyperinsulinemia.
Article in The Journal of biological chemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.
- The crucial role and mechanism of insulin resistance in metabolic disease.Frontiers in endocrinology · 2023Pooled it
- Mitigation of Oxidative Stress Pathways in the Diabetic Cornea and Lacrimal Glands Contributes to the Rapid Reversal of Diabetic Dry Eye by Naltrexone.Investigative ophthalmology & visual science · 2026Article
- Association Between CBC-Derived Inflammatory Indicators and 28-Day Mortality in Patients With Coronary Heart Disease and Diabetes Mellitus: A Cohort Study From the MIMIC-IV Database.Mediators of inflammation · 2026Article
- Efficacy of Addiction Pharmacotherapy in Alcohol Use Disorder and Their Effects on Liver Health.Journal of clinical and translational hepatology · 2024Review
- Association between dietary insulin index and postmenopausal osteoporosis in Iranian women: a case-control study.BMC women's health · 2024Article
- Article
- Molecular pathways dysregulated by PbToxicology research · 2022Article
- LDN Protects Bone Property Deterioration at Different Hierarchical Levels in T2DM Mice Bone.ACS omega · 2021Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The incidence of diabetes, obesity, and metabolic diseases has reached an epidemic status worldwide. Insulin resistance is a common link in the development of these conditions, and hyperinsulinemia is a central hallmark of peripheral insulin resistance. However, how hyperinsulinemia leads to systemic insulin resistance is less clear. We now provide evidence that hyperinsulinemia promotes the release of soluble pro-inflammatory mediators from macrophages that lead to systemic insulin resistance. Our observations suggest that hyperinsulinemia induces sirtuin1 (SIRT1) repression and stimulates NF-κB p65 nuclear translocation and transactivation of NF-κB to promote the extracellular release of pro-inflammatory mediators. We further showed that low-dose naltrexone (LDN) abrogates hyperinsulinemia-mediated SIRT1 repression and prevents NF-κB p65 nuclear translocation. This, in turn, attenuates the hyperinsulinemia-induced release of pro-inflammatory cytokines and reinstates insulin sensitivity both in
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Registered trials
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.