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During liver development, there are physiological changes, from the predominant utilization of glucose (fetal life) to the use of lipids (postnatal life). Fasting is another physiological stress that elicits well\u2010known metabolic adjustments. We have reported the metabolic properties of cardiotrophin\u20101 (CT\u20101), a member of the interleukin\u20106 family of cytokines. Here, we aimed at analyzing the role of CT\u20101 in response to these metabolic changes. We used different in vivo models. Furthermore, a differential study was carried out with wild\u2010type and CT\u20101 null mice in fed (ad libitum) and food\u2010restricted conditions. We demonstrated that\n                    <jats:italic>Ct\u20101<\/jats:italic>\n                    is a metabolic gene induced in the liver via PPAR\u03b1 in response to lipids in mice (neonates\u2010 and food\u2010restricted adults). We found that\n                    <jats:italic>Ct\u20101<\/jats:italic>\n                    mRNA expression in white adipose tissue directly involved PPAR\u03b1 and PPAR\u03b3. Finally, the physiological role of CT\u20101 in fasting is confirmed by the impaired food restriction\u2010induced adipose tissue lipid mobilization in CT\u20101 null mice. Our findings support a previously unrecognized physiological role of CT\u20101 in metabolic adaptations, through the regulation of lipid metabolism and contributes to fasting\u2010induced free fatty acid mobilization.\n                  <\/jats:p>","DOI":"10.1096\/fj.202000109r","type":"journal-article","created":{"date-parts":[[2020,10,13]],"date-time":"2020-10-13T03:01:17Z","timestamp":1602558077000},"page":"15875-15887","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Cardiotrophin\u20101 contributes to metabolic adaptations through the regulation of lipid metabolism and to the fasting\u2010induced fatty acid mobilization"],"prefix":"10.1096","volume":"34","author":[{"given":"David","family":"Carneros","sequence":"first","affiliation":[{"name":"Area of Liver, Digestive and Inflammatory Diseases, Institute of Biomedicine of Seville (IBiS) Consejo Superior de Investigaciones Cient\u00edficas (CSIC) University of Seville, Virgen del Rocio University Hospital Seville Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gema","family":"Medina\u2010G\u00f3mez","sequence":"additional","affiliation":[{"name":"Department of Basic Sciences of Health, Area of Biochemistry and Molecular Biology Rey Juan Carlos University Madrid Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marta","family":"Giralt","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Molecular Biomedicine Barcelona University Barcelona Spain"},{"name":"CIBERobn Physiopathology of Obesity and Nutrition, Institute of Health Carlos III (ISCIII) Madrid Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Manuel","family":"Le\u00f3n\u2010Camacho","sequence":"additional","affiliation":[{"name":"Department of Lipid Characterization and Quality Instituto de la Grasa (CSIC) Seville 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