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. Author manuscript; available in PMC: 2020 Nov 10.
Published in final edited form as: J Mol Endocrinol. 2020 Feb;64(2):53–65. doi: 10.1530/JME-19-0053

Figure 5.

Figure 5

Gastrin synthesis, D1R, and PPAR-α in SW626 and human G cells. (A) Monensin (MON, 1 μM/24 h) or fenofibrate (FFB, PPAR-α agonist, 5 μM/30 min) increases gastrin protein in SW626 cells (IF, immunofluorescence; RFU, relative fluorescence units) (*P < 0.05 vs vehicle (VEH/24 h), one-way ANOVA, Tukey test). GW6471 (GW, PPAR-α antagonist, 5 μM/30 min) decreases gastrin protein (#P < 0.05, vs VEH, FFB, one-way ANOVA, Tukey test) and prevents the stimulatory effect of FFB but not MON on gastrin protein ($P < 0.001 vs others, one-way ANOVA, Tukey test). n = 10/group. (B) FFB (5 μM/30 min) increases gastrin protein in isolated human G cells (relative fluorescence units, RFU) (**P < 0.01, vs others, one-way ANOVA, Tukey test, n = 6/group). GW6471 (GW, PPAR-α antagonist, 5 μM/30 min) and LE300 (D1-like receptor antagonist, 10 μM/30 min), by themselves, do not affect gastrin protein expression but prevent the stimulatory effect of FFB on gastrin protein expression (*P < 0.05, vs FFB, one-way ANOVA, Tukey test, n = 6/group).