Maletti M, Altman J J, Hoa D H, Carlquist M, Rosselin G
Fondation de Recherche en Hormonologie, Fresnes, France.
Diabetes. 1987 Nov;36(11):1336-40. doi: 10.2337/diab.36.11.1336.
Specific gastric inhibitory polypeptide (GIP) receptors were characterized in human benign insulinoma plasma membranes employing [mono-[125I]iodo-Tyr10]-GIP (125I-GIP) as the radioligand. GIP 1-42 inhibited 125I-GIP binding with an IC50 value of 10(-9) M. Scatchard analysis showed two classes of binding sites: a high-affinity site (Kd = 2.23 x 10(-10) M; Bmax = 24 fmol/mg protein) and a low-affinity site (Kd = 8.39 x 10(-9) M; Bmax = 118 fmol/mg protein). A synthetic replicate of human GIP 1-31 inhibited 125I-GIP binding with an IC50 value of 10(-8) M. The GIP binding sites of human insulinoma were coupled to adenylate cyclase stimulation. GIP 1-31 regulated the adenylate cyclase activity to the same extent as GIP 1-42. The concentrations of GIP required for maximal activity ranged from 10(-9) to 10(-8) M for either GIP 1-42 or GIP 1-31. The existence of functional GIP receptors in human insulinoma substantiates our recent reports demonstrating the presence of GIP binding sites in transplantable hamster insulinoma and indicates that GIP could exert a direct control of the beta-cell function in humans through a purely endocrine pathway.
利用[单-[125I]碘代-Tyr10]-GIP（125I-GIP）作为放射性配体，对人良性胰岛素瘤质膜中的特异性胃抑制多肽（GIP）受体进行了表征。GIP 1-42以10^(-9) M的IC50值抑制125I-GIP结合。Scatchard分析显示有两类结合位点：一个高亲和力位点（Kd = 2.23×10^(-10) M；Bmax = 24 fmol/mg蛋白）和一个低亲和力位点（Kd = 8.39×10^(-9) M；Bmax = 118 fmol/mg蛋白）。人GIP 1-31的合成复制品以10^(-8) M的IC50值抑制125I-GIP结合。人胰岛素瘤的GIP结合位点与腺苷酸环化酶刺激相偶联。GIP 1-31调节腺苷酸环化酶活性的程度与GIP 1-42相同。对于GIP 1-42或GIP 1-31，最大活性所需的GIP浓度范围为10^(-9)至10^(-8) M。人胰岛素瘤中功能性GIP受体的存在证实了我们最近的报道，即证明了可移植仓鼠胰岛素瘤中存在GIP结合位点，并表明GIP可能通过纯粹的内分泌途径对人类β细胞功能发挥直接控制作用。
