Associations of FGF23 and Apelin-13 with osteoporosis and diabetic peripheral neuropathy in postmenopausal women with type 2 diabetes mellitus.
To investigate the correlations of various clinical indicators, fibroblast growth factor 23 (FGF23), and Apelin-13 with osteoporosis (OP) and diabetic peripheral neuropathy (DPN) in postmenopausal women with type 2 diabetes mellitus (T2DM), and to evaluate their predictive value for OP and DPN.
A total of 320 postmenopausal women were enrolled, including 238 patients with T2DM and 82 non-diabetic patients with OP. Clinical data, bone metabolism markers, continuous glucose monitoring parameters, Current Perception Threshold (CPT), and Bone Mineral Density (BMD) were collected. Serum levels of FGF23 and Apelin-13 were measured via ELISA. Multivariate regression analyses identified independent factors for BMD, OP, and DPN in T2DM patients. Predictive performance was evaluated using ROC curves. The characteristic clinical phenotype of OP patients with comorbid T2DM was also summarized.
In postmenopausal women with T2DM, 25OH-VitD and Apelin-13 were independently associated with higher T-scores (protective factors), while PTH, CPT scores, and FGF23 were independently associated with lower T-scores (risk factors). Logistic regression revealed that longer DD, elevated superficial peroneal/saphenous nerve CPT scores, and higher FGF23 were independently associated with increased OP risk, while higher E2 and Apelin-13 were independently associated with decreased OP risk. The combined model of these indicators showed an AUC of 0.958 (95% CI: 0.934-0.982) for predicting OP. Logistic regression indicated that a lower BMD T-score was independently associated with increased DPN risk (OR = 0.13, p < 0.001), with a predictive AUC of 0.926 (95% CI: 0.891-0.961). OP patients with T2DM exhibited a more adverse metabolic-bone profile, including higher FGF23 and lower Apelin-13.
In this cross-sectional study, decreased BMD in postmenopausal T2DM women was independently associated with bone metabolism disorders, FGF23/Apelin-13 imbalance, and impaired nerve function. OP and DPN shared long diabetes duration, high FGF23, and low Apelin-13. A model combining DD, E2, CPT, FGF23, and Apelin-13 showed good OP discrimination (AUC = 0.958); BMD T-score discriminated DPN (AUC = 0.926). Both require external validation. These hypothesis-generating findings suggest that FGF23 and Apelin-13 may be potential targets for future research on synergistic OP/DPN prevention and treatment.
A total of 320 postmenopausal women were enrolled, including 238 patients with T2DM and 82 non-diabetic patients with OP. Clinical data, bone metabolism markers, continuous glucose monitoring parameters, Current Perception Threshold (CPT), and Bone Mineral Density (BMD) were collected. Serum levels of FGF23 and Apelin-13 were measured via ELISA. Multivariate regression analyses identified independent factors for BMD, OP, and DPN in T2DM patients. Predictive performance was evaluated using ROC curves. The characteristic clinical phenotype of OP patients with comorbid T2DM was also summarized.
In postmenopausal women with T2DM, 25OH-VitD and Apelin-13 were independently associated with higher T-scores (protective factors), while PTH, CPT scores, and FGF23 were independently associated with lower T-scores (risk factors). Logistic regression revealed that longer DD, elevated superficial peroneal/saphenous nerve CPT scores, and higher FGF23 were independently associated with increased OP risk, while higher E2 and Apelin-13 were independently associated with decreased OP risk. The combined model of these indicators showed an AUC of 0.958 (95% CI: 0.934-0.982) for predicting OP. Logistic regression indicated that a lower BMD T-score was independently associated with increased DPN risk (OR = 0.13, p < 0.001), with a predictive AUC of 0.926 (95% CI: 0.891-0.961). OP patients with T2DM exhibited a more adverse metabolic-bone profile, including higher FGF23 and lower Apelin-13.
In this cross-sectional study, decreased BMD in postmenopausal T2DM women was independently associated with bone metabolism disorders, FGF23/Apelin-13 imbalance, and impaired nerve function. OP and DPN shared long diabetes duration, high FGF23, and low Apelin-13. A model combining DD, E2, CPT, FGF23, and Apelin-13 showed good OP discrimination (AUC = 0.958); BMD T-score discriminated DPN (AUC = 0.926). Both require external validation. These hypothesis-generating findings suggest that FGF23 and Apelin-13 may be potential targets for future research on synergistic OP/DPN prevention and treatment.