ArticleMolecular medicine reports2026
Effects of zinc carnosine on bone loss in mice with diabetic osteoporosis.
Article in Molecular medicine reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Diabetic osteoporosis (DOP) is on the rise globally, presenting a notable healthcare challenge due to its complex pathogenesis and high fracture risk. Currently, available treatments have limitations, highlighting an urgent need for novel therapeutic approaches. Zinc carnosine (ZnC), a compound formed by the chelation of carnosine with trace‑element zinc ions, has shown potential in inhibiting the accumulation of advanced glycation end products in the bone microenvironment, yet its effects on DOP remain under‑explored. The present study aimed to examine the effects of ZnC on bone loss in a mouse model of DOP. A total of 24 male mice, aged 6 weeks, were assigned to control, type 2 diabetes mellitus (T2DM) and ZnC intervention groups. DOP was induced using a high‑fat diet combined with streptozotocin (STZ). Following 8 weeks of treatment with ZnC at a dosage of 100 mg/kg/day, bone parameters were evaluated using micro‑computed tomography (micro‑CT), histological staining and molecular analyses. The micro‑CT analysis revealed that bone mineral density (BMD), bone volume/tissue volume (BV/TV), number of bone trabeculae (Tb.N), thickness of cortical bone (Ct.Th) and area of cortical bone (Ct.Ar) were significantly lower in the T2DM model group compared with that in the control group (P<0.05). Conversely, bone trabecular separation (Tb.Sp) structural model index (SMI) and porosity of cortical bone (Ct.Po) were significantly higher in the T2DM model group compared with those in the control group (P<0.05). The ZnC intervention group showed significant increases in BMD, BV/TV, Tb.N, Ct.Th and Ct.Ar, and significant decreases in Tb.Sp compared with the T2DM model group. Tartrate‑resistant acid phosphatase staining demonstrated a notable reduction in osteoclast numbers in the ZnC intervention group relative to the T2DM model group. Furthermore, immunohistochemical staining and reverse transcription‑quantitative PCR indicated an upregulation of osteoblastic markers, including type Ⅰ collagen, osteocalcin and osteoprotegerin, alongside a downregulation of the osteoclastic marker receptor activator of nuclear factor‑κB ligand in the ZnC group. In conclusion, ZnC supplementation was shown to mitigate bone loss in DOP by promoting bone formation and reducing bone resorption. This was evidenced by enhancements in bone microstructure, a reduction in osteoclast activity and favorable changes in bone metabolism markers. These findings underscore the potential of ZnC as a therapeutic option for bone diseases associated with diabetes.
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