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. 2007 Aug 27;104(38):15069–15074. doi: 10.1073/pnas.0706890104

Fig. 3.

Fig. 3.

Secretion of GLP-1 in response to glucose, sucrose, and sucralose in NCI-H716 cells. (A and B) Glucose-, sucrose-, and sucralose-mediated GLP-1 secretion from NCI-H716 cells. The sweet receptor inhibitor lactisole inhibited sucralose-mediated GLP-1 secretion. (C) siRNA-mediated diminution of both α-gustducin protein levels (by immunoblotting) and glucose-induced [but not basal (BSL)] GLP-1 secretion from NCI-H716 cells. (D) Immunoblotting of ERK and pERK phosphorylated from NCI-H716 cells in response to increasing concentrations of glucose and sucralose. The inhibitor of Erk phosphorylation, PD98059, inhibited sucralose-mediated Erk phosphorylation. The sweet receptor inhibitor lactisole diminished Erk phosphorylation. BSL, basal. Experiments were carried out in triplicate and replicated at least twice. Statistical significance determined by ANOVA; values are means ± SEM; *, P < 0.05; ***, P < 0.001.