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The pancreatic islets comprising only 1%-2% of the volume are highly vascularized and innervated mini-organs. They contain five endocrine cell types, including β cells that secrete insulin, which is synthesized as a single polypeptide chain, preproinsulin, processed to proinsulin, and finally to insulin and C-peptide. This process is complex and regulated, involving the Golgi complex, the endoplasmic reticulum, and the secretory granules of the β cell.
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The endoplasmic reticulum (ER) of pancreatic β-cells synthesizes preproinsulin, which consists of a signal peptide, A and B chains, and a C-peptide. Preproinsulin is then cleaved and folded into proinsulin, which translocates to the Golgi apparatus for sorting and packaging into secretory granules. In these granules, enzymatic clipping generates insulin and C-peptide.
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La secreción de insulina en las células β requiere la ubiquitina ligasa COP1

Rowena Suriben1, Kelly A Kaihara2, Magdalena Paolino1

  • 1Department of Physiological Chemistry, Genentech, 1 DNA Way, South San Francisco, CA 94080, USA.

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|December 3, 2015
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Resumen

La ubiquitina ligasa COP1 regula los factores de transcripción de ETV en las células beta pancreáticas, lo cual es crucial para la secreción de insulina y la prevención de la diabetes. La eliminación de estos factores salva la diabetes, destacando su papel en la homeostasis de la glucosa.

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Área de la Ciencia:

  • Endocrinología
  • Biología molecular
  • Biología celular

Sus antecedentes:

  • Las células beta del páncreas secretan insulina para mantener la homeostasis de la glucosa en sangre.
  • La secreción desregulada de insulina contribuye a la diabetes.
  • Las modificaciones posteriores a la traducción regulan los procesos celulares clave.

Objetivo del estudio:

  • Investigar el papel de la regulación post-traducional mediada por COP1 de los factores de transcripción de ETV en las células beta pancreáticas.
  • Determinar el impacto de esta regulación en la secreción de insulina y la homeostasis de la glucosa.

Principales métodos:

  • Los ratones generados carecen de COP1 en las células beta.
  • Se ha realizado la eliminación genética de Etv1, Etv4 y Etv5.
  • Análisis de la secreción de insulina y acoplamiento de gránulos.
  • Examinó los patrones de expresión génica.

Principales resultados:

  • La pérdida de COP1 en las células beta condujo a la diabetes debido al deterioro del acoplamiento de los gránulos de insulina.
  • La eliminación genética de Etv1, Etv4 y Etv5 rescató el fenotipo diabético.
  • Los genes regulados por las ETV en las células con deficiencia de COP1 se enriquecieron en genes asociados a la diabetes humana.
  • ETV4 se estabilizó tras la despolarización y la secreción limitada de insulina durante la hiperglucemia.

Conclusiones:

  • La regulación mediada por COP1 de los factores de transcripción de ETV es crítica para la secreción de insulina y el mantenimiento de la normoglucemia.
  • Los ETV actúan como reguladores negativos de la secreción de insulina, especialmente en condiciones de hiperglucemia.
  • Estos hallazgos sugieren un papel conservado para las ETV en la fisiopatología de las células beta humanas y la diabetes.