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La señalización "vasocrina" de la grasa perivascular: un mecanismo que vincula la resistencia a la insulina con la

John S Yudkin¹, Etto Eringa, Coen D A Stehouwer

¹Diabetes and Cardiovascular Disease Academic Unit, Department of Medicine, Royal Free and University College Medical School, The Archway Campus, Holborn Union Building, 2-10 Highgate Hill, London N19 5LW, UK. j.yudkin@ucl.ac.uk

Lancet (London, England)

|May 25, 2005

Resumen

La obesidad perjudica los efectos de los vasos sanguíneos de la insulina debido a los depósitos de grasa que liberan el factor de necrosis tumoral alfa. Esto causa vasoconstricción, lo que dificulta la capacidad de la insulina para ensanchar los vasos sanguíneos.

Área de la Ciencia:

Fisiología Fisiología Fisiología.
Endocrinología Endocrinología.
Biología Vascular Biología Vascular

Sus antecedentes:

El tejido adiposo libera citoquinas que afectan la señalización de la insulina en el hígado y el músculo.
La obesidad está relacionada con el deterioro de la vasodilatación mediada por insulina.
Los depósitos de grasa locales cerca de las arteriolas pueden desempeñar un papel vasorregulador.

Objetivo del estudio:

Para investigar el papel vasorregulador de la grasa periarteriolar en las arteriolas del músculo esquelético.
Aclarar los mecanismos de la vasodilatación y vasoconstricción mediadas por insulina.
Para explorar el impacto de la obesidad en estas respuestas vasculares.

Principales métodos:

Aislamiento de arteriolas de primer orden del músculo cremaster de la rata.
Evaluación de los efectos de la insulina en las vías de la endotelina-1 y del óxido nítrico (NO).
Análisis de la participación de la adipocitocina (factor de necrosis tumoral alfa) en las arteriolas de ratas obesas.

Principales resultados:

La insulina ejerce una regulación dual: vasoconstricción mediada por endotelina-1 y vasodilatación mediada por NO.
Las arteriolas de ratas obesas muestran deterioro de la síntesis de NO estimulada por insulina, lo que lleva a una vasoconstricción sin oposición.
El factor de necrosis tumoral alfa de la grasa periarteriolar está implicado en esta alteración de la vasodilatación.

Conclusiones:

Los depósitos de grasa periarteriolar en la obesidad producen el factor de necrosis tumoral alfa, que causa vasoconstricción.
La señalización "vasocrina" por esta citoquina inhibe el reclutamiento capilar mediado por insulina.
Este mecanismo puede vincular la grasa visceral, la resistencia a la insulina y las enfermedades vasculares.

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