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Inositolphosphoglycans possibly mediate the effects of glucagon‐like peptide‐1(7‐36)amide on rat liver and adipose tissue
Author(s) -
Márquez Luis,
Trapote María A.,
Luque Miguel A.,
Valverde I.,
VillanuevaPeñacarrillo María L.
Publication year - 1998
Publication title -
cell biochemistry and function
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.933
H-Index - 61
eISSN - 1099-0844
pISSN - 0263-6484
DOI - 10.1002/(sici)1099-0844(199803)16:1<51::aid-cbf767>3.0.co;2-t
Subject(s) - endocrinology , adipose tissue , medicine , skeletal muscle , glucagon , insulin , receptor , biology , chemistry
Insulin‐like effects of glucagon‐like peptide‐1(7‐36)amide (GLP‐1) in rat liver, skeletal muscle and fat, and also the presence of GLP‐1 receptors in these extrapancreatic tissues, have been documented. In skeletal muscle and liver, the action of GLP‐1 is not associated with an activation of adenylate cyclase, and in cultured murine myocytes and hepatoma cell lines, it was found that GLP‐1 provokes the generation of inositolphosphoglycan molecules (IPGs), which are considered second messengers of insulin action. In the present work, we document in isolated normal rat adipocytes and hepatocytes that GLP‐1 exerts a rapid decrease of the radiolabelled glycosylphosphatidylinositols (GPIs)—precursors of IPGs—in the same manner as insulin, indicating their hydrolysis and the immediate short‐lived generation of IPGs. Thus, IPGs could be mediators in the GLP‐1 actions in adipose tissue and liver, as well as in skeletal muscle, through GLP‐1 receptors which are, at least functionally, different from that of the pancreatic B‐cell. © 1998 John Wiley & Sons, Ltd.