Alaa Jameel A. Albarakati

Diabetic osteoporosis is a major complication of Type 1 Diabetes Mellitus (T1DM), driven by hyperglycemia, oxidative stress, inflammation, and apoptosis of osteogenic cells. This study investigated the protective role of coenzyme Q10 (CoQ10) on bone loss in a rat model of T1DM. Forty male Wistar rats were divided into four groups: control, CoQ10 alone, untreated diabetic, and diabetic treated with CoQ10 (50 mg/kg/day for 8 weeks). Diabetes was induced by streptozotocin injection. We performed biochemical, histological, and molecular analyses. Results showed that diabetic rats exhibited hyperglycemia, reduced osteocalcin, elevated bone resorption markers (CTX-1, TRACP 5b), and dysregulated regulatory proteins (RUNX2, OPG, RANKL). Histological examination revealed trabecular bone loss and marrow cavity expansion. CoQ10 supplementation significantly enhanced osteogenic activity, suppressed osteoclast function, and restored trabecular architecture. Antioxidant enzyme activities (SOD, CAT, GPx) were markedly improved in CoQ10-treated diabetic rats. Moreover, CoQ10 downregulated the TLR4/NF-κB signaling pathway and decreased proinflammatory cytokines (TNF-α, IL-6, IL-1β). Apoptotic markers (Bax and caspase-3) were reduced, while the anti-apoptotic protein Bcl-2 was elevated, confirming the anti-apoptotic effect of CoQ10. In conclusion, CoQ10 supplementation mitigates diabetes-induced bone loss through antioxidant, anti-inflammatory, and antiapoptotic mechanisms. These findings highlight CoQ10 as a promising adjunctive therapy for preserving bone health in T1DM.

KEY WORDS: Diabetes mellitus; Coenzyme Q10; Osteogenic; Oxidative stress; Inflammation; Apoptosis.

ALBARAKATI, A. J. A. Protective effect of coenzyme Q10 on diabetic bone loss by targeting oxidative stress, and TLR4/NFκB pathway. Int. J. Morphol., 44(3):738-746, 2026.