ArticleMolecular medicine reports2016
Interruptin B induces brown adipocyte differentiation and glucose consumption in adipose-derived stem cells.
Article in Molecular medicine reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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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.
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Who cites it
6 citing papers in PubMed, 12 citations in OpenAlex.
- Interruptins Extracted fromNutrients · 2025Article
- Cyclosorus Terminans Extract Alleviates Neuroinflammation in Insulin Resistant Rats.Molecular neurobiology · 2024Article
- Antioxidative and Anti-photooxidative Potential of Interruptins from the Edible FernCurrent pharmaceutical biotechnology · 2024Article
- Article
- MD001, a Novel Peroxisome Proliferator-activated Receptor α/γ Agonist, Improves Glucose and Lipid Metabolism.Scientific reports · 2019Article
- Adipose tissue stem cells in regenerative medicine.Ecancermedicalscience · 2018Review
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interruptin B has been isolated from Cyclosorus terminans, however, its pharamcological effect has not been fully identified. In the present study, the effects of interruptin B, from C. terminans, on brown adipocyte differentiation and glucose uptake in adipose‑derived stem cells (ASCs) were investigated. The results revealed that interruptin B dose‑dependently enhanced the adipogenic differentiation of ASCs, with an induction in the mRNA expression levels of peroxisome proliferator‑activated receptor (PPAR)‑α and PPAR‑γ. In addition, interruptin B efficiently increased the number and the membrane potential of mitochondria and upregulated the mRNA expression levels of uncoupling protein (UCP)‑1 and cyclooxygenase (COX)‑2, which are all predominantly expressed in brown adipocytes. Interruptin B increased glucose consumption in differentiated ASCs, accompanied by the upregulation in the mRNA expression levels of glucose transporter (GLUT)‑1 and GLUT‑4. The computational analysis of molecular docking, a luciferase reporter assay and surface plasmon resonance confirmed the marked binding affinity of interruptin B to PPAR‑α and PPAR‑γ (K(D) values of 5.32 and 0.10 µm, respectively). To the best of our knowledge, the present study is the first report to show the stimulatory effects of interruptin B on brown adipocyte differentiation and glucose uptake in ASCs, through its role as a dual PPAR‑α and PPAR‑γ ligand. Therefore, interruptin B could be further developed as a therapeutic agent for the treatment of diabetes.
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