N-glycosylation regulates GIP receptor number and GIP-potentiated insulin secretion in INS-1 cells.

<p>(<b>A</b>) Plot of specific binding versus concentration of ¹²⁵I-GIP saturation carried out in INS-1 cells with or without 1 µg/ml tunicamycin. Data were fitted with a non-linear regression equation assuming a single binding site (GraphPad Prism). Control cells expressed an average of 2443±400 GIP receptors on the cell surface (Kd 455±50 pM), whereas tunicamycin-treated cells expressed 760±70 GIP receptors on the cell surface (Kd 345±100 pM). (<b>B</b>) Plot of insulin release in response to glucose and/or GIP, from INS-1 cells with or without 1 µg/ml tunicamycin. Data are expressed as mean ± SEM, n = 4 separate experiments. Asterisk indicates a significant increase in insulin release compared to basal conditions without addition of 50 nM GIP (P<0.05), as determined using two-way ANOVA followed by Bonferroni post-tests.