Sobre la asociación entre el hígado graso no alcohólico y la insulinorresistencia

Mildred Rosario Díaz Morales, Celia Alonso Rodríguez, Pedro Velbes Marquetti, Tania Hidalgo Costa

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Justificación: La insulinorresistencia (IR) se imbrica de muchas maneras con el hígado graso no alcohólico (HGNA). Es muy probable que el HGNA se acompañe de estados de IR. Objetivo: Establecer la presencia de IR en pacientes con HGNA. Diseño del estudio: Analítico, transversal. Serie de estudio: Cincuenta pacientes (Mujeres: 58.0%; Piel blanca: 76.0%; Edades promedio:
53.0 ± 12.4 años; Índice de Masa Corporal: 30.4 ± 4.6 Kg.m-2) diagnosticados con HGNA (Afectación: Grave: 6.0%; Moderada: 54.0%; Leve: 40.0%) mediante ultrasonografía (US) en el Servicio de Gastroenterología del Hospital Clínico quirúrgico “Hermanos Ameijeiras” (La Habana, Cuba). Material y método: Se determinaron las concentraciones séricas de triglicéridos, colesterol total y fraccionado, enzimas hepáticas, y glucosa e insulina en ayunas y 2 horas después de una sobrecarga oral de glucosa (SCOG). Adicionalmente, se calcularon los cocientes ASAT/ALAT y GGT/ASAT; y los índices HOMA-IR, HOMA-β, y de sensibilidad a la insulina (ISI). Se evaluó la naturaleza de las asociaciones entre las variables bioquímicas determinadas y la gravedad del HGNA. Resultados: El HGNA se asoció con valores elevados de la actividad GGT (y por extensión, el índice GGT/ASAT). Igualmente, el HGNA se asoció con cifras elevadas de glucosa en ayunas y 2 horas después de la SCOG. El HGNA se acompañó también de incremento del producto plasmático Glucosa*Insulina en ayunas (dado por el comportamiento del índice HOMA-R) y después de la SCOG (como sugiere la disminución del índice IS). Conclusiones: En el HGNA concurren daño hepático y resistencia a la insulina. Estos 2 factores actuando de
conjunto pueden resultar en daño orgánico permanente.

Palabras clave

Obesidad; Hígado graso no alcohólico; Ultrasonido; Insulinorresistencia

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