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    Por favor, use este identificador para citar o enlazar este ítem: http://hdl.handle.net/10259/4965

    Título
    Liver-specific ablation of insulin-degrading enzyme causes hepatic insulin resistance and glucose intolerance, without affecting insulin clearance in mice
    Autor
    Villa Pérez, Pablo .
    Merino, Beatriz .
    Fernández Díaz, Cristina M. .
    Cidad, Pilar .
    Lobatón, Carmen D. .
    Moreno, Alfredo .
    Muturi, Harrison T. .
    Ghadieh, Hilda E. .
    Najjar, Sonia M. .
    Leissring, Malcolm A. .
    Cózar Castellano, Irene .
    Perdomo Hernández, Germán M.UBU authority
    Publicado en
    Metabolism. 2018, V. 88, p. 1-11
    Editorial
    Elsevier
    Fecha de publicación
    2018-11
    ISSN
    0026-0495
    DOI
    10.1016/j.metabol.2018.08.001
    Abstract
    The role of insulin-degrading enzyme (IDE), a metalloprotease with high affinity for insulin, in insulin clearance remains poorly understood. OBJECTIVE: This study aimed to clarify whether IDE is a major mediator of insulin clearance, and to define its role in the etiology of hepatic insulin resistance. Methods We generated mice with liver-specific deletion of Ide (L-IDE-KO) and assessed insulin clearance and action. Results L-IDE-KO mice exhibited higher (~20%) fasting and non-fasting plasma glucose levels, glucose intolerance and insulin resistance. This phenotype was associated with ~30% lower plasma membrane insulin receptor levels in liver, as well as ~55% reduction in insulin-stimulated phosphorylation of the insulin receptor, and its downstream signaling molecules, AKT1 and AKT2 (reduced by ~40%). In addition, FoxO1 was aberrantly distributed in cellular nuclei, in parallel with up-regulation of the gluconeogenic genes Pck1 and G6pc. Surprisingly, L-IDE-KO mice showed similar plasma insulin levels and hepatic insulin clearance as control mice, despite reduced phosphorylation of the carcinoembryonic antigen-related cell adhesion molecule 1, which upon its insulin-stimulated phosphorylation, promotes receptor-mediated insulin uptake to be degraded. Conclusion IDE is not a rate-limiting regulator of plasma insulin levels in vivo
    Palabras clave
    nsulin-degrading enzyme
    Hepatic insulin resistance
    Insulin recepto
    Carcinoembryonic antigen-related cell adhesion molecule 1
    Materia
    Endocrinología
    Endocrinology
    URI
    http://hdl.handle.net/10259/4965
    Versión del editor
    https://doi.org/10.1016/j.metabol.2018.08.001
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