ArticleInternational journal of molecular sciences2023
Denosumab Attenuates Glucolipotoxicity-Induced β-Cell Dysfunction and Apoptosis by Attenuating RANK/RANKL Signals.
Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Effects of a single-dose denosumab on glucose and lipid homeostasis in young infertile men.Endocrine · 2026Trial
- Drug Repurposing in Oncology: A Strategic Pathway to Unlocking New Therapeutic Potential.Therapeutic innovation & regulatory science · 2026Review
- Osteoporosis After Menopause and After Drug Therapy: The Molecular Mechanism of Bone Loss and Its Treatment.International journal of molecular sciences · 2026Review
- The role of bone in whole-body energy metabolism.Nature reviews. Endocrinology · 2025Review
- Role of denosumab in lipid metabolism disorders: clinical significance and potential mechanisms.Archives of osteoporosis · 2025Review
- Therapeutic effects and mechanisms of Xinmaitong formula for type 2 diabetes mellitus via GLP-1R signaling.Frontiers in pharmacology · 2025Article
- Trabecular Bone Score (TBS) in Individuals with Type 2 Diabetes Mellitus: An Updated Review.Journal of clinical medicine · 2023Review
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Obesity is strongly associated with insulin sensitivity in type 2 diabetes (T2D), mainly because free fatty acids (FFAs) are released from excess fat tissue. Long-term exposure to high levels of FFAs and glucose leads to glucolipotoxicity, causing damage to pancreatic β-cells, thus accelerating the progression of T2D. Therefore, the prevention of β-cell dysfunction and apoptosis is essential to prevent the development of T2D. Unfortunately, there are currently no specific clinical strategies for protecting β-cells, highlighting the need for effective therapies or preventive approaches to improve the survival of β-cells in T2D. Interestingly, recent studies have shown that the monoclonal antibody denosumab (DMB), used in osteoporosis, displays a positive effect on blood glucose regulation in patients with T2D. DMB acts as an osteoprotegerin (OPG) by inhibiting the receptor activator of the NF-κB ligand (RANKL), preventing the maturation and function of osteoclasts. However, the exact mechanism by which the RANK/RANKL signal affects glucose homeostasis has not been fully explained. The present study used human 1.4 × 10
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