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Our data show that postnatal increase in COUP-TFII mRNA levels is enhanced by glucagon (via cAMP) and PPAR\u03b1. To characterize COUP-TFII function in the liver of suckling mice, we used a functional (dominant negative form; COUP-TFII-DN) and a genetic (shRNA) approach. Adenoviral COUP-TFII-DN injection induces a profound hypoglycemia due to the inhibition of gluconeogenesis and fatty acid oxidation secondarily to reduced PEPCK, Gl-6-Pase, CPT I, and mHMG-CoA synthase gene expression. Using the crossover plot technique, we show that gluconeogenesis is inhibited at two different levels: 1) pyruvate carboxylation and 2) trioses phosphate synthesis. This could result from a decreased availability in fatty acid oxidation arising cofactors such as acetyl-CoA and reduced equivalents. Similar results are observed using the shRNA approach. Indeed, when fatty acid oxidation is rescued in response to Wy-14643-induced PPAR\u03b1 target genes (CPT I and mHMG-CoA synthase), blood glucose is normalized in COUP-TFII-DN mice. In conclusion, this work demonstrates that postnatal increase in hepatic COUP-TFII gene expression is involved in the regulation of liver fatty acid oxidation, which in turn sustains an active hepatic gluconeogenesis that is essential to maintain an appropriate blood glucose level required for newborn mice survival.<\/jats:p>","DOI":"10.1152\/ajpendo.00433.2014","type":"journal-article","created":{"date-parts":[[2015,3,18]],"date-time":"2015-03-18T02:58:44Z","timestamp":1426647524000},"page":"E868-E878","source":"Crossref","is-referenced-by-count":13,"title":["The role of chicken ovalbumin upstream promoter transcription factor II in the regulation of hepatic fatty acid oxidation and gluconeogenesis in newborn mice"],"prefix":"10.1152","volume":"308","author":[{"given":"Julien","family":"Planchais","sequence":"first","affiliation":[{"name":"Institut National de la Sante et de la Recherche Medicale, U1016, Institut Cochin, Paris, France;"},{"name":"Centre National de la Recherche 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