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Functional assays using ex vivo liver tissue sections demonstrate that Klf11\u2212\/\u2212 mice display increased insulin sensitivity. Genome-wide experiments validated by pathway-specific quantitative PCR arrays reveal that the Klf11\u2212\/\u2212 phenotype associates to alterations in the regulation of gene networks involved in lipid metabolism, in particular those regulated by peroxisome proliferator-activated receptor-\u03b3. Combined, these results demonstrate that the major phenotype given by the whole-body deletion of Klf11 in mouse is not diabetes but increased insulin sensitivity, likely due to altered transcriptional regulation in target tissues. The absence of diabetes in the Klf11\u2212\/\u2212 mouse either indicates an interspecies difference for the role of this transcription factor in metabolic homeostasis between mouse and humans, or potentially highlights the fact that other molecular factors can compensate for its absence. Nevertheless, the data of this study, gathered at the whole-organism level, further support a role for KLF11 in metabolic processes like insulin sensitivity, which regulation is critical in several forms of diabetes.<\/jats:p>","DOI":"10.1210\/en.2015-1145","type":"journal-article","created":{"date-parts":[[2015,8,6]],"date-time":"2015-08-06T17:47:00Z","timestamp":1438883220000},"page":"3581-3595","source":"Crossref","is-referenced-by-count":13,"title":["Phenotypic Characterization of Mice Carrying Homozygous Deletion of KLF11, a Gene in Which Mutations Cause Human Neonatal and MODY VII Diabetes"],"prefix":"10.1210","volume":"156","author":[{"given":"Angela","family":"Mathison","sequence":"first","affiliation":[{"name":"Laboratory of Epigenetics and Chromatin Dynamics (A.M., A.S., W.A.F., N.B., G.L., R.U.), Gastroenterology Research Unit, Departments of Biochemistry and Molecular Biology, Biophysics, Medicine, Epigenomics Translation Program Center for Individualized Medicine, Mayo 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