
Introduction:
Polycystic ovary syndrome (PCOS) has been associated with conflicting effects on bone mass, underscoring the need for deeper investigation into its impact on skeletal health. This study aimed to assess the expression of osteoporosis-related genes in femoral bone, alongside hormonal profile (bone-related hormones) alterations, across aging in a rat model of PCOS compared to controls.
Materials and methods:
Femoral bone RNA was extracted from rat model of PCOS and controls (n = 10-13 per group) at 3, 10, and 18 months of age. The expression of IL-11, DKK1, RANKL, AKT1, IGF-1, EphB4, STAT3, and CTNNB1 genes was quantified via Real-Time PCR. Concurrently, serum levels of Anti-Mullerian Hormone (AMH), calcitonin, cortisol, total testosterone (TT), and vitamin D3 were measured using ELISA.
Results:
A significantly elevated expression of IL-11, DKK1, RANKL, AKT1, and IGF-1 genes, accompanied by a decreased expression of EphB4 and STAT3 in the femoral bone of rat model of PCOS compared to controls, was observed. Additionally, rat model of PCOS exhibited higher serum levels of AMH, cortisol, and TT, whereas calcitonin and vitamin D3 levels were decreased.
Conclusions:
These molecular and hormonal alterations highlight a dysregulation in bone metabolism associated with PCOS and suggest that PCOS may represent a substantial risk factor for osteoporosis later in life. The employed rat model thus offers a valuable platform for elucidating the cellular and molecular mechanisms contributing to bone mass disorders in PCOS, facilitating the development of targeted therapeutic strategies.
Keywords:
Bone; Gene; Hormone; Osteoporosis; Polycystic ovary syndrome.
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