Liver glucokinase: An overview on the regulatorymechanisms of its activity

Authors

  • María L. Massa,

    1. CENEXA, Centro de Endocrinología Experimental y Aplicada (UNLP-CONICET LA PLATA, Centro Colaborador OPS/OMS), Facultad de Ciencias Médicas, 60 y 120, 1900 La Plata, Argentina
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  • Juan J. Gagliardino,

    1. CENEXA, Centro de Endocrinología Experimental y Aplicada (UNLP-CONICET LA PLATA, Centro Colaborador OPS/OMS), Facultad de Ciencias Médicas, 60 y 120, 1900 La Plata, Argentina
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  • Flavio Francini

    Corresponding author
    1. CENEXA, Centro de Endocrinología Experimental y Aplicada (UNLP-CONICET LA PLATA, Centro Colaborador OPS/OMS), Facultad de Ciencias Médicas, 60 y 120, 1900 La Plata, Argentina
    • CENEXA (UNLP-CONICET LA PLATA), Facultad de Ciencias Médicas, Calles 60 y 120, 1900 La Plata Argentina
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    • Tel.: +54-221-423-6712. Fax: +54-221-422-20-81


Abstract

Blood glucose is the primary cellular substrate and in vivo must be tightly maintained. The liver plays a key role in glucose homeostasis increasing or decreasing glucose output and uptake during fasting and feeding. Glucokinase (GCK) is central to this process. Its activity is modulated in a coordinated manner via a complex set of mechanisms: in the postprandial period, the simultaneous rise in glucose and insulin increases GCK activity by enhanced gene expression, changes in cellular location, and interaction with regulatory proteins. Conversely, in the fasting state, the combined decrease in glucose and insulin concentrations and increase in glucagon concentrations, halt GCK activity. Herein we summarize the current knowledge regarding the regulation of hepatic GCK activity. © 2011 IUBMB IUBMB Life, 63(1): 1–6, 2011

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