Frontiers in immunology · 2026
Immune cells and high-density lipoprotein cholesterol derivative markers mediate the impact of hypertriglyceridemia on hyperuricemia in diabetes mellitus.
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Wang Wei, Qiu Xiu Ping, Chen Yang, Guo Xiu Li
Аннотация
BACKGROUND: As markers of inflammation and oxidative stress, immune cells and high-density lipoprotein cholesterol (HDL-c) derivative markers, such as the monocyte to HDL-c ratio (MHR) and lymphocyte to HDL-c ratio (LHR), have been widely utilized in clinical practice. This study aims to elucidate the roles of MHR and LHR in the impact of hypertriglyceridemia (HTG) on hyperuricemia (HUA) in diabetes mellitus (DM) from a clinical perspective.
METHODS: The final analysis included 976 individuals with DM. The correlations of MHR and LHR with HTG and HUA were evaluated using the restricted cubic splines (RCS) and binomial logistic regression analysis. Additionally, the mediating role of MHR and LHR in the effect of HTG on HUA was assessed using an adjusted mediation analysis.
RESULTS: Participants in the HTG and HUA groups demonstrated significantly elevated MHR and LHR levels (All P < 0.001). After applying adjustment for potential confounders, MHR remained a significant association with HTG and HUA, with ORs (95% CI) of 1.59 (1.43-1.77) for HTG and 1.13 (1.04-1.23) for HUA (both P < 0.05). Similarly, LHR exhibited independent correlations with HTG and HUA, yielding ORs (95% CI) of 2.34 (1.91-2.88) for HTG and 1.63 (1.33-2.00) for HUA. In the RCS analysis, MHR exhibited a nonlinear relationship with both HTG (P for nonlinear = 0.001) and HUA (P for nonlinear < 0.001). Conversely, LHR demonstrated a linear correlation with HTG (P for nonlinear = 0.062) and HUA (P for nonlinear = 0.268). Furthermore, the adjusted mediation analysis revealed that both MHR and LHR partially mediated the effect of HTG on HUA, accounting for the mediated proportion of 20.51% and 37.17%, respectively.
CONCLUSION: Both MHR and LHR partially mediate the effect of HTG on HUA, indicating the vital effect of inflammation and oxidative stress in this association.
METHODS: The final analysis included 976 individuals with DM. The correlations of MHR and LHR with HTG and HUA were evaluated using the restricted cubic splines (RCS) and binomial logistic regression analysis. Additionally, the mediating role of MHR and LHR in the effect of HTG on HUA was assessed using an adjusted mediation analysis.
RESULTS: Participants in the HTG and HUA groups demonstrated significantly elevated MHR and LHR levels (All P < 0.001). After applying adjustment for potential confounders, MHR remained a significant association with HTG and HUA, with ORs (95% CI) of 1.59 (1.43-1.77) for HTG and 1.13 (1.04-1.23) for HUA (both P < 0.05). Similarly, LHR exhibited independent correlations with HTG and HUA, yielding ORs (95% CI) of 2.34 (1.91-2.88) for HTG and 1.63 (1.33-2.00) for HUA. In the RCS analysis, MHR exhibited a nonlinear relationship with both HTG (P for nonlinear = 0.001) and HUA (P for nonlinear < 0.001). Conversely, LHR demonstrated a linear correlation with HTG (P for nonlinear = 0.062) and HUA (P for nonlinear = 0.268). Furthermore, the adjusted mediation analysis revealed that both MHR and LHR partially mediated the effect of HTG on HUA, accounting for the mediated proportion of 20.51% and 37.17%, respectively.
CONCLUSION: Both MHR and LHR partially mediate the effect of HTG on HUA, indicating the vital effect of inflammation and oxidative stress in this association.