Experimental eye research · 2025
The role of metabolic factors in the causal association between body mass index and cataract: A Mendelian randomization mediation analysis.
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Liu Jingjing, Du Shanshan, Shao Jingzhi, Qi Ying, Zhang Fengyan
Аннотация
OBJECTIVE: To investigate the mediating roles of metabolic factors, encompassing type 2 diabetes (T2D), C-reactive protein (CRP), and interleukin-6 (IL-6), in the causality between body mass index (BMI) and cataract, thereby elucidating potential mechanisms underlying obesity-related cataractogenesis.
METHODS: Utilizing European population-based genome-wide association study (GWAS) data, a two-step Mendelian randomization (MR) analysis and a multivariable MR (MVMR) were undertaken to assess mediation effects. The two-step MR approach was leveraged to examine whether T2D, CRP, and IL-6 mediated the link between BMI and cataract, while MVMR was utilized to quantify the direct causal effects of these mediating factors.
RESULTS: The two-step MR results unraveled that BMI was linked to an elevated likelihood of developing cataract (OR = 1.17, 95 % CI: 1.11-1.22, p = 3.25 × 10-10). T2D was established as a potential mediator in the link between BMI and cataract (OR = 1.125, 95 % CI: 1.106-1.144, p = 1.22 × 10-33). No statistically significant associations were found between either CRP or IL-6 and cataract risk. The MVMR results revealed a significant direct effect of T2D on cataract (OR = 1.12, 95 % CI: 1.09-1.16, p < 1 × 10-17), while the direct effect of BMI was not statistically significant (OR = 1.04, 95 % CI: 0.98-1.10, p = 0.12). These findings suggested that T2D served as the core pathway through which BMI influenced the development of cataract.
CONCLUSION: Obesity-associated cataract is primarily mediated by T2D. Enhancing glycemic control in obese populations may effectively prevent this condition.
TRANSLATIONAL RELEVANCE: We identify type 2 diabetes (T2D) as the primary mediator in the link between obesity and cataract via genetic epidemiology, shifting clinical prevention toward glycemic control for high-BMI populations.
METHODS: Utilizing European population-based genome-wide association study (GWAS) data, a two-step Mendelian randomization (MR) analysis and a multivariable MR (MVMR) were undertaken to assess mediation effects. The two-step MR approach was leveraged to examine whether T2D, CRP, and IL-6 mediated the link between BMI and cataract, while MVMR was utilized to quantify the direct causal effects of these mediating factors.
RESULTS: The two-step MR results unraveled that BMI was linked to an elevated likelihood of developing cataract (OR = 1.17, 95 % CI: 1.11-1.22, p = 3.25 × 10-10). T2D was established as a potential mediator in the link between BMI and cataract (OR = 1.125, 95 % CI: 1.106-1.144, p = 1.22 × 10-33). No statistically significant associations were found between either CRP or IL-6 and cataract risk. The MVMR results revealed a significant direct effect of T2D on cataract (OR = 1.12, 95 % CI: 1.09-1.16, p < 1 × 10-17), while the direct effect of BMI was not statistically significant (OR = 1.04, 95 % CI: 0.98-1.10, p = 0.12). These findings suggested that T2D served as the core pathway through which BMI influenced the development of cataract.
CONCLUSION: Obesity-associated cataract is primarily mediated by T2D. Enhancing glycemic control in obese populations may effectively prevent this condition.
TRANSLATIONAL RELEVANCE: We identify type 2 diabetes (T2D) as the primary mediator in the link between obesity and cataract via genetic epidemiology, shifting clinical prevention toward glycemic control for high-BMI populations.