{"title":"El rol modulador de lesiones en sustancia blanca en la mediación entre IMC, lípidos, presión arterial y niveles de glucosa","authors":"Alberto Guevara Tirado","doi":"10.1016/j.neuarg.2025.06.005","DOIUrl":null,"url":null,"abstract":"<div><h3>Introduction</h3><div>Cardiometabolic alterations affect glycemic control, but the modulatory role of cerebral white matter lesions in these associations is not yet fully understood.</div></div><div><h3>Objective</h3><div>To evaluate whether the presence of cerebral white matter lesions moderates the relationship between BMI and glucose through cardiometabolic markers.</div></div><div><h3>Materials and Methods</h3><div>Analytical secondary data study (n<!--> <!-->=<!--> <!-->1904) of patients undergoing clinical evaluations and brain MRI. The independent variable was BMI and fasting glucose the dependent variable; mediators included LDL, triglycerides (TG), and systolic blood pressure (SBP); and the moderator was the presence of cerebral white matter lesions. Hayes’ PROCESS model 59 was used to assess direct, indirect, and moderated effects. The causal model was visualized with a directed acyclic graph.</div></div><div><h3>Results</h3><div>The effect of BMI on LDL (β<!--> <!-->=<!--> <!-->1.47; p<!--> <!--><<!--> <!-->0.001), TG (β<!--> <!-->=<!--> <!-->10.13; p<!--> <!--><<!--> <!-->0.001), and SBP(β<!--> <!-->=<!--> <!-->1.45; p<!--> <!--><<!--> <!-->0.001) was attenuated in the presence of lesions, with significant negative interactions (LDL: β<!--> <!-->=<!--> <!-->−0.86; p<!--> <!-->=<!--> <!-->0.036; TG: β<!--> <!-->=<!--> <!-->−3.89; p<!--> <!-->=<!--> <!-->0.003; SBP: β<!--> <!-->=<!--> <!-->−0.81; p<!--> <!-->=<!--> <!-->0.001). In the glucose model, BMI (β<!--> <!-->=<!--> <!-->1.36; p<!--> <!--><<!--> <!-->0.001), TG (β<!--> <!-->=<!--> <!-->0.015; p<!--> <!-->=<!--> <!-->0.003), and SBP (β<!--> <!-->=<!--> <!-->0.11; p<!--> <!-->=<!--> <!-->0.004) showed positive associations. Lesions had no significant direct effect (β<!--> <!-->=<!--> <!-->11.58; p<!--> <!-->=<!--> <!-->0.12) but moderated the BMI-glucose (interaction: β<!--> <!-->=<!--> <!-->−0.49; p<!--> <!-->=<!--> <!-->0.048) and TG-glucose (interaction: β<!--> <!-->=<!--> <!-->0.058; p<!--> <!--><<!--> <!-->0.001) relationships. The indirect effect of BMI on glucose via triglycerides was greater in the presence of lesions (β<!--> <!-->=<!--> <!-->0.45; 95%<span>C</span>I: 0.25–0.75) than in their absence (β<!--> <!-->=<!--> <!-->0.15;95%CI: 0.01-0.40). Mediation through SBP was significant in both groups (no lesions: β<!--> <!-->=<!--> <!-->0.15; with lesions: β<!--> <!-->=<!--> <!-->0.07).</div></div><div><h3>Conclusions</h3><div>The indirect effects of BMI on glucose are modulated by the presence of cerebral white matter lesions, highlighting the modulatory role of brain damage in the pathways linking adiposity and glycemic control.</div></div>","PeriodicalId":39051,"journal":{"name":"Neurologia Argentina","volume":"17 3","pages":"Pages 173-180"},"PeriodicalIF":0.0000,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Neurologia Argentina","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S1853002825000400","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"Medicine","Score":null,"Total":0}
引用次数: 0
Abstract
Introduction
Cardiometabolic alterations affect glycemic control, but the modulatory role of cerebral white matter lesions in these associations is not yet fully understood.
Objective
To evaluate whether the presence of cerebral white matter lesions moderates the relationship between BMI and glucose through cardiometabolic markers.
Materials and Methods
Analytical secondary data study (n = 1904) of patients undergoing clinical evaluations and brain MRI. The independent variable was BMI and fasting glucose the dependent variable; mediators included LDL, triglycerides (TG), and systolic blood pressure (SBP); and the moderator was the presence of cerebral white matter lesions. Hayes’ PROCESS model 59 was used to assess direct, indirect, and moderated effects. The causal model was visualized with a directed acyclic graph.
Results
The effect of BMI on LDL (β = 1.47; p < 0.001), TG (β = 10.13; p < 0.001), and SBP(β = 1.45; p < 0.001) was attenuated in the presence of lesions, with significant negative interactions (LDL: β = −0.86; p = 0.036; TG: β = −3.89; p = 0.003; SBP: β = −0.81; p = 0.001). In the glucose model, BMI (β = 1.36; p < 0.001), TG (β = 0.015; p = 0.003), and SBP (β = 0.11; p = 0.004) showed positive associations. Lesions had no significant direct effect (β = 11.58; p = 0.12) but moderated the BMI-glucose (interaction: β = −0.49; p = 0.048) and TG-glucose (interaction: β = 0.058; p < 0.001) relationships. The indirect effect of BMI on glucose via triglycerides was greater in the presence of lesions (β = 0.45; 95%CI: 0.25–0.75) than in their absence (β = 0.15;95%CI: 0.01-0.40). Mediation through SBP was significant in both groups (no lesions: β = 0.15; with lesions: β = 0.07).
Conclusions
The indirect effects of BMI on glucose are modulated by the presence of cerebral white matter lesions, highlighting the modulatory role of brain damage in the pathways linking adiposity and glycemic control.
期刊介绍:
Neurología Argentina es la publicación oficial de la Sociedad Neurológica Argentina. Todos los artículos, publicados en español, son sometidos a un proceso de revisión sobre ciego por pares con la finalidad de ofrecer información original, relevante y de alta calidad que abarca todos los aspectos de la Neurología y la Neurociencia.