Establishment of novel specific assay for short‐form glucose‐dependent insulinotropic polypeptide and evaluation of its secretion in nondiabetic subjects. Issue 11 (29th May 2020)

• Record Type: Journal Article
• Authors: Takeda, Yasutaka; Fujita, Yukihiro; Yanagimachi, Tsuyoshi; Maruyama, Nobuhiro; Bessho, Ryoichi; Sakagami, Hidemitsu; Honjo, Jun; Yokoyama, Hiroki; Haneda, Masakazu
• Is Part Of: Physiological reports. Volume 8:Issue 11(2020)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2020-05-29
• Subjects: cookie meal test -- DPP‐4 inhibitor -- ELISA -- GIP (1–30) -- oral glucose tolerance test; Physiology -- Periodicals; 571
• DOI: 10.14814/phy2.14469
• Languages: English
• ISSNs: 2051-817X

Abstract

Abstract: The short‐form glucose‐dependent insulinotropic polypeptide (GIP) (1–30) is released from islet alpha cells and promotes insulin secretion in a paracrine manner in vitro. However, it is not well elucidated how GIP (1–30) is involved in glucose metabolism in vivo, since a specific assay system for GIP (1–30) has not yet been established. We first developed a sandwich enzyme‐linked immunosorbent assay (ELISA) specific for GIP (1–30) by combining a novel antibody specific to the GIP (1–30) C terminus with the common antibody against GIP N terminus. Then, we explored cross‐reactivities with incretins and glucagon‐related peptides in this ELISA. GIP (1–30) amide, but not GIP (1–42), GLP‐1, or glucagon increased absorbance in a dose‐dependent manner. We next measured plasma GIP (1–30) concentrations in nondiabetic participants (ND) during a 75‐g oral glucose tolerance test or cookie meal test (carbohydrates 75 g, lipids 28.5 g, proteins 8.5 g). Both glucose and cookie load increased GIP (1–30) concentrations in ND, but the increases were much lower than those of GIP (1–42). Furthermore, the DPP‐4 inhibitor significantly increased GIP (1–30) concentrations similarly to GIP (1–42) in ND. In conclusion, we for the first time developed an ELISA specific for GIP (1–30) and revealed its secretion in ND. Abstract : For the first time, we established a novel ELISA specific for GIP (1–30). GIP (1–30) secretion is promoted by oral glucose and mix meal load in nondiabetics. DPP‐4 inhibitors increased peripheral blood GIP (1–30) levels.