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. 2014 Dec 11;9(6):2219–2232. doi: 10.1016/j.celrep.2014.11.033

Figure 3.

Figure 3

The Deletion of Rfx6 in β Cells Causes Glucose Intolerance due to Defective Insulin Secretion

(A–C) Exploration of glucose metabolism in adult (12- to 14-week-old) controls (n = 8) and Rfx6ΔBeta (n = 7) males under normal diet 4 weeks after tamoxifen injections. Blood glucose levels are measured in overnight (16 hr)-fasted and ad libitum-fed animals 1 month after tamoxifen injections (A). Intraperitoneal glucose tolerance test (IPGTT) after 16 hr fasting in male mice 1 month after tamoxifen injections (B). Oral glucose tolerance test (OGTT) after 16 hr fasting in male mice 1 month after tamoxifen injections (C).

(D) Histogram representing the plasma insulin levels of control and Rfx6ΔBeta mice (9–11 weeks old) during an in vivo glucose-stimulated insulin secretion test (n = 6) performed 5 days after tamoxifen injections.

(E) Histogram representing the insulin released during an ex vivo glucose- and KCl-stimulated insulin secretion tests on islets purified from controls and Rfx6ΔBeta (n = 4) mice (9–11 weeks old), 5 days after tamoxifen injections.

Data are presented as mean ± SD; p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.