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Loss-of-Function Mutation of theGPR40Gene Associates with Abnormal Stimulated Insulin Secretion by Acting on Intracellular Calcium Mobilization
Author(s) -
Roberto Vettor,
Marnie Granzotto,
Diego De Stefani,
Elisabetta Trevellin,
Marco Rossato,
Maria Grazia Farina,
Gabriella Milan,
Catia Pilon,
A. Nigro,
Giovanni Federspil,
Riccardo Vigneri,
Libero Vitiello,
Rosario Rizzuto,
Roberto Baratta,
Lucia Frittitta
Publication year - 2008
Publication title -
the journal of clinical endocrinology and metabolism
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.206
H-Index - 353
eISSN - 1945-7197
pISSN - 0021-972X
DOI - 10.1210/jc.2007-2680
Subject(s) - calcium in biology , intracellular , secretion , mobilization , function (biology) , insulin , mutation , endocrinology , calcium , gene , medicine , free fatty acid receptor 1 , microbiology and biotechnology , biology , receptor , genetics , agonist , history , archaeology
Free fatty acids (FFAs) acutely stimulate but chronically impair glucose-stimulated insulin secretion from beta-cells. The G protein-coupled transmembrane receptor 40 (GPR40) mediates both acute and chronic effects of FFAs on insulin secretion and plays a role in glucose homeostasis. Limited information is available on the effect of GPR40 genetic abnormalities on insulin secretion and metabolic regulation in human subjects.

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