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. 2016 Mar 23;157(5):1866–1880. doi: 10.1210/en.2015-2010

Figure 7.

Figure 7.

Selective deletion of Gprc6a in pancreatic β-cell attenuated insulin, Srebp1c, and Chrebp expression but not glucagon expression in pancreas. Comparison of insulin (A) and glucagon (B) expression in pancreas from in control group and Gprc6aβ-cell-cko mice. C, Comparison of Srebp1c and Chrebp expression in pancreas and liver from in control group and Gprc6aβ-cell-cko mice. Expression was assessed by real-time PCR using total RNA derived from pancreas or liver from control group and Gprc6aβ-cell-cko mice. Insulin, glucagon, Srebp1c, and Chrebp expression is relative to the level of the cyclophilin control gene. Comparison of insulin (D) and glucagon (E) expression in pancreatic islets. Expression was assessed by real-time PCR using total RNA derived from isolated islets from control group and Gprc6aβ-cell-cko mice. Insulin and glucagon expression is relative to the level of the cyclophilin control gene. F, Comparison of Srebp1c and Chrebp expression in isolated islets from control and Gprc6aβ-cell-cko mice. Expression of insulin, Srebp1c, and Chrebp, but not glucagon, were significantly different in islets from Gprc6aβ-cell-cko mice compared with the islets from control group mice. G, Expression of GPRC6A transcript in INS-1 β-cells. The expected sized fragment was generated from 3 different primer sets for gprc6a, set 1–2 spanning exons 1 and 2 of 438-bp length, set 3–4 spanning exons 3 and 4 of 865 bp, and set 5–6 spanning exons 5–6 of 572 bp. Dose-dependent effects of Ocn on GPRC6A-mediated ERK phosphorylation (H) and insulin secretion (I) in INS-1 β-cells. Values represent the mean ± SEM. *, significant difference between control group and Gprc6aβ-cell-cko mice (P < .05; n ≥ 3).