Skip to main content
. 2015 Mar 30;4:e06253. doi: 10.7554/eLife.06253

Figure 2. Glucagon (GCG) receptor regulates phase resetting effects of OXM and GCG in Per2::LUC liver slices.

(A) OXM-induced phase shifts in Per2::LUC and Per2::LUC x Glp1r−/− liver slices. Mann–Whitney test: ##p < 0.01 against solvent. (B) GCG and OXM-induced phase shifts in Per2::LUC slices are abolished by co-treatment with GRI-2. One-way ANOVA with Bonferroni post-test: p < 0.05; ###p < 0.001 against solvent; *p < 0.05; ***p < 0.001. Data are presented as mean ± S.E.M. (n = 8); F(7, 56) = 7.314. (C) OXM treatment promotes binding of CREB to CRE elements at the Per1 gene promoter. One-way ANOVA with Bonferroni post-test: ***p < 0.001 against 0′. Data are presented as mean ± S.E.M. (n = 5; F(5, 24) = 22.2).

DOI: http://dx.doi.org/10.7554/eLife.06253.006

Figure 2.

Figure 2—figure supplement 1. Absence of Glp1r transcripts in mouse liver.

Figure 2—figure supplement 1.

RT-PCR with different primer sets targeting all annotated coding exons of the murine Glp1r gene. Exon 1 was not tested, as it mainly contains non-coding poly-C- and poly-G-rich sequences, which precludes specific primer design. cDNA preparations from wild-type livers were tested (lane 2). Wild-type pancreas cDNA was chosen as positive (lane 4) and liver cDNA from Glp1r-deficient mice and water as negative controls (lanes 3 and 5). Lane 1: 100-bp DNA ladder.