ArticleFrontiers in endocrinology2020
Hyperbaric Oxygen Ameliorates Insulin Sensitivity by Increasing GLUT4 Expression in Skeletal Muscle and Stimulating UCP1 in Brown Adipose Tissue in T2DM Mice.
Article in Frontiers in endocrinology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 28 citations in OpenAlex.
- Trial
- Decreased adipose tissue oxygenation associates with insulin resistance in individuals with obesity.The Journal of clinical investigation · 2020Trial
- The SUMO specific peptidase SENP3 promotes papillary thyroid cancer progression by deSUMOylation of SETDB1 and regulating GLI2 transcription.Clinical and experimental medicine · 2026Article
- Review of Hyperbaric Oxygen Therapy as an Adjunctive Intervention for Metabolic Disorders.Antioxidants (Basel, Switzerland) · 2025Review
- A pathophysiological intersection between metabolic biomarkers and memory: a longitudinal study in the STZ-induced diabetic mouse model.Frontiers in physiology · 2025Article
- Endothelial Dysfunction and Cardiovascular Disease: Hyperbaric Oxygen Therapy as an Emerging Therapeutic Modality?Journal of cardiovascular development and disease · 2024Review
- Potency of Hyperbaric Oxygen Therapy on Oral Candidiasis Diabetes Mellitus.European journal of dentistry · 2024Article
- Complex Hippocampal Response to Thermal Skin Injury and Protocols with Hyperbaric Oxygen Therapy andInternational journal of molecular sciences · 2024Article
- Hyperbaric oxygen therapy for healthy aging: From mechanisms to therapeutics.Redox biology · 2022Review
- Hyperbaric oxygen treatment improves pancreatic β‑cell function and hepatic gluconeogenesis in STZ‑induced type‑2 diabetes mellitus model mice.Molecular medicine reports · 2022Article
- The Effect of Hyperbaric Therapy on Brown Adipose Tissue in Rats.International journal of environmental research and public health · 2021Article
- Hyperbaric oxygen therapy affects insulin sensitivity/resistance by increasing adiponectin, resistin, and plasminogen activator inhibitor-I in ratsTurkish journal of medical sciences · 2021Article
- Natural Extracts to Augment Energy Expenditure as a Complementary Approach to Tackle Obesity and Associated Metabolic Alterations.Biomolecules · 2021Article
- Diagnostic significance of serum PP4R1 and its predictive value for the development of chronic complications in patients with type 2 diabetes mellitus.Diabetology & metabolic syndrome · 2021Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hyperbaric oxygen (HBO) therapy is a treatment modality useful for diseases. Hypoxia could stimulate the induction of insulin resistance. Therefore, we sought to determine whether hyperbaric oxygen would ameliorate insulin sensitivity by promoting glucose transporter type 4 (GLUT4) expression in muscle and by stimulating UCP1 in brown adipose tissue (BAT) in a streptozocin (STZ)-induced type 2 diabetes mellitus (T2DM) mouse model. Male C57BL/6J mice were treated three times with low-dose of streptozocin (60 mg/kg, i.p.) and were fed with high-fat diets (HFD) to establish the T2DM model. HBO was administered daily as 100% oxygen at 2.0 atmosphere absolute (ATA) for 1 h for a week. We found that HBO significantly reduced blood glucose levels and attenuated insulin resistance in T2DM mice. HBO modulated food intake by influencing the activity of neuropeptide Y (NPY)-positive neurons in the arcuate nucleus (Arc). HBO treatment increased GLUT4 amount and level of phosphorylated Akt (p-Akt) in muscles of T2DM mice whereas this treatment stimulated the phosphorylation of AMPK in muscles of both T2DM and HFD mice. The morphological staining of BAT and the increased expression of uncoupling of protein 1 (UCP1) demonstrated the promotion of metabolism after HBO treatment. These findings suggest that HBO ameliorates insulin sensitivity of T2DM mice by stimulating the Akt signaling pathway and by promoting GLUT4 expression in muscle, and by increasing UCP1 expression in BAT.
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