Neftali Eduardo Antonio-Villa1, Omar Yaxmehen Bello-Chavolla2, Arsenio Vargas-Vázquez1, Roopa Mehta3, Carlos A Fermín-Martínez1, Alexandro J Martagón-Rosado4, Daphne Abigail Barquera-Guevara5, Carlos A Aguilar-Salinas6. 1. Unidad de Investigación de Enfermedades Metabólicas, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City, Mexico; MD/PhD (PECEM) Program, Facultad de Medicina, Universidad Nacional Autónoma de México, Mexico City, Mexico. 2. Unidad de Investigación de Enfermedades Metabólicas, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City, Mexico; División de Investigación, Instituto Nacional de Geriatría, Mexico City, Mexico. 3. Unidad de Investigación de Enfermedades Metabólicas, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City, Mexico; Departamento de Endocrinología y Metabolismo del Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City, Mexico. 4. Unidad de Investigación de Enfermedades Metabólicas, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City, Mexico; Tecnologico de Monterrey, Escuela de Medicina y Ciencias de la Salud, Mexico City, Mexico. 5. Unidad de Investigación de Enfermedades Metabólicas, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City, Mexico; Programa AFINES, Facultad de Medicina, Universidad Nacional Autónoma de México, Mexico City, Mexico. 6. Unidad de Investigación de Enfermedades Metabólicas, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City, Mexico; Departamento de Endocrinología y Metabolismo del Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City, Mexico; Tecnologico de Monterrey, Escuela de Medicina y Ciencias de la Salud, Mexico City, Mexico. Electronic address: caguilarsalinas@yahoo.com.
Abstract
BACKGROUND AND AIMS: Both insulin resistance (IR) and visceral adipose tissue (VAT) are related cardiometabolic risk factors; nevertheless, their joint effect on endothelial functionality is controversial. This study aims to evaluate the joint effect of IR and VAT on endothelial functionality using the pulse-waveform analysis and explore the mediating role of VAT on the effect of IR on arterial pressure, arterial stiffness and incident arterial hypertension. METHODS AND RESULTS: We measured VAT (n = 586) using two methods (dual-energy X-ray absorptiometry and a clinical surrogate), arterial stiffness (with pulse-waveform velocity), and IR (using three methods: HOMA2-IR (n = 586), a frequently sampled intravenous glucose tolerance test (n = 131) and euglycemic hyperinsulinemic clamping (n = 97)) to confirm the mediator effect of IR on VAT. The incidence of arterial hypertension attributable to the mediating effect of IR related to VAT was evaluated using a prospective cohort (n = 6850). Adjusted linear regression models, causal mediation analysis, and Cox-proportional hazard risk regression models were performed to test our objective. IR and VAT led to increased arterial stiffness and increased blood pressure; the combination of both further worsened vascular parameters. Nearly, 57% (ΔE→MY 95% CI: 31.7-100.0) of the effect of IR on altered pulse-wave velocity (PWV) analysis was mediated through VAT. Moreover, VAT acts as a mediator of the effect of IR on increased mean arterial pressure (ΔE→MY 35.7%, 95% CI: 23.8-59) and increased hypertension risk (ΔE→MY 69.1%, 95% CI: 46.1-78.8). CONCLUSION: VAT acts as a mediator of IR in promoting arterial stiffness and arterial hypertension. Both phenomena should be targeted to ameliorate the cardiometabolic risk.
BACKGROUND AND AIMS: Both insulin resistance (IR) and visceral adipose tissue (VAT) are related cardiometabolic risk factors; nevertheless, their joint effect on endothelial functionality is controversial. This study aims to evaluate the joint effect of IR and VAT on endothelial functionality using the pulse-waveform analysis and explore the mediating role of VAT on the effect of IR on arterial pressure, arterial stiffness and incident arterial hypertension. METHODS AND RESULTS: We measured VAT (n = 586) using two methods (dual-energy X-ray absorptiometry and a clinical surrogate), arterial stiffness (with pulse-waveform velocity), and IR (using three methods: HOMA2-IR (n = 586), a frequently sampled intravenous glucose tolerance test (n = 131) and euglycemic hyperinsulinemic clamping (n = 97)) to confirm the mediator effect of IR on VAT. The incidence of arterial hypertension attributable to the mediating effect of IR related to VAT was evaluated using a prospective cohort (n = 6850). Adjusted linear regression models, causal mediation analysis, and Cox-proportional hazard risk regression models were performed to test our objective. IR and VAT led to increased arterial stiffness and increased blood pressure; the combination of both further worsened vascular parameters. Nearly, 57% (ΔE→MY 95% CI: 31.7-100.0) of the effect of IR on altered pulse-wave velocity (PWV) analysis was mediated through VAT. Moreover, VAT acts as a mediator of the effect of IR on increased mean arterial pressure (ΔE→MY 35.7%, 95% CI: 23.8-59) and increased hypertension risk (ΔE→MY 69.1%, 95% CI: 46.1-78.8). CONCLUSION: VAT acts as a mediator of IR in promoting arterial stiffness and arterial hypertension. Both phenomena should be targeted to ameliorate the cardiometabolic risk.
Authors: Monika Starzak; Agata Stanek; Grzegorz K Jakubiak; Armand Cholewka; Grzegorz Cieślar Journal: Int J Environ Res Public Health Date: 2022-08-19 Impact factor: 4.614
Authors: Alexandro J Martagón; Carlos A Fermín-Martínez; Neftali Eduardo Antonio-Villa; Roopa Mehta; Paloma Almeda-Valdés; Arsenio Vargas-Vázquez; Liliana Muñoz-Hernández; Donají V Gómez-Velasco; Daniel Elías-López; Gabriela A Galán-Ramírez; Fabiola Mabel Del Razo-Olvera; Ivette Cruz-Bautista; Rogelio González-Arellanes; Carlos A Aguilar-Salinas Journal: Int J Environ Res Public Health Date: 2022-09-03 Impact factor: 4.614