Open AccessNovel extrapancreatic effects of incretin
Author(s) -
Yamada Yuichiro,
Tsukiyama Katsushi,
Sato Takehiro,
Shimizu Tatsunori,
Fujita Hiroki,
Narita Takuma
Publication year - 2016
Publication title -
journal of diabetes investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.089
H-Index - 50
eISSN - 2040-1124
pISSN - 2040-1116
DOI - 10.1111/jdi.12495
Subject(s) - incretin , gastric inhibitory polypeptide , glucagon like peptide 1 , medicine , endocrinology , receptor , dipeptidyl peptidase 4 , dipeptidyl peptidase , glucagon like peptide 1 receptor , hormone , gastrointestinal hormone , diabetes mellitus , glucagon , peptide hormone , type 2 diabetes , biology , biochemistry , enzyme , agonist
Abstract The hormonal factors implicated as transmitters of signals from the gut to pancreatic β‐cells are referred to as incretins. Gastric inhibitory polypeptide ( GIP ) and glucagon‐like peptide‐1 ( GLP ‐1) are incretins. In addition to the insulinotropic effects, we have shown, using the GIP receptor and GLP ‐1 receptor‐deficient mice, that GIP and GLP ‐1 have direct actions on adipocytes and the kidney, respectively. Because GIP receptors and GLP ‐1 receptors are differentially expressed in a tissue‐specific manner, GIP and GLP ‐1 have specific physiological activities, and further comprehensive characterization of the extrapancreatic actions of GIP and GLP ‐1 is anticipated, as dipeptidyl peptidase IV inhibitors activate both GIP and GLP ‐1 signaling.