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. 2023 Jun 1;37(11-12):490–504. doi: 10.1101/gad.350569.123

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© 2023 Abarinov et al.; Published by Cold Spring Harbor Laboratory Press

This article, published in Genes & Development, is available under a Creative Commons License (Attribution 4.0 International), as described at http://creativecommons.org/licenses/by/4.0/.

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Figure 5. — RIP-Cre;Nkx2.2^SDmut/flox (βSDmut) animals develop diabetes due to impaired β cell function. (A) Schematic of alleles used to generate βSDmut mice. (B,C) Body weight (B) and ad lib blood glucose levels (C) in male βSDmut animals. (D) βSDmut males show elevated fasting blood glucose levels and impaired glucose clearance at 4 wk compared with littermate RIP-Cre;Nkx2.2^flox/+ control animals (CTRLS) during the intraperitoneal glucose tolerance test (IP-GTT). (E) INS, SST, and PP expression in 4-wk βSDmut animals. (F–K) RNA-seq analysis of NKX2.2-bound genes that are significantly altered in βSDmut islets versus CTRLS compared with NKX2.2-bound genes that are significantly altered in RIP-Cre;Nkx2.2^flox/flox (βKO) animals versus CTRLS. (F) Gene ontology (GO) analysis of the 70 genes bound by NKX2.2 and down-regulated in both βSDmut and βKO islets compared with CTRL mice. (G) FPKM values of selected genes from F. (H) GO analysis of the 62 genes bound by NKX2.2 and up-regulated in both βSDmut and βKO versus CTRL animals. (I) FPKM values of selected genes from H. (J) GO analysis of the 346 transcripts bound by NKX2.2 and only up-regulated in βSDmut animals. (K) Schematic comparing differences in islet morphology and function in βKO versus βSDmut mice. Data are presented as mean ± SEM. (ns) Not significant, (*) P < 0.05, (**) P < 0.01, (***) P < 0.001. Scale bars represent 50 µm.