It is becoming clear that several human pathologies are caused by altered metabolic adaptations. 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‐known metabolic adjustments. We have reported the metabolic properties of cardiotrophin‐1 (CT‐1), a member of the interleukin‐6 family of cytokines. Here, we aimed at analyzing the role of CT‐1 in response to these metabolic changes. We used different in vivo models. Furthermore, a differential study was carried out with wild‐type and CT‐1 null mice in fed (ad libitum) and food‐restricted conditions. We demonstrated that Ct‐1 is a metabolic gene induced in the liver via PPARα in response to lipids in mice (neonates‐ and food‐restricted adults). We found that Ct‐1 mRNA expression in white adipose tissue directly involved PPARα and PPARγ. Finally, the physiological role of CT‐1 in fasting is confirmed by the impaired food restriction‐induced adipose tissue lipid mobilization in CT‐1 null mice. Our findings support a previously unrecognized physiological role of CT‐1 in metabolic adaptations, through the regulation of lipid metabolism and contributes to fasting‐induced free fatty acid mobilization.

中文翻译：

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Cardiotrophin-1 通过调节脂质代谢和禁食诱导的脂肪酸动员促进代谢适应

越来越清楚的是，几种人类病理是由代谢适应性改变引起的。在肝脏发育过程中，存在生理变化，从主要利用葡萄糖（胎儿生命）到利用脂质（出生后生命）。禁食是另一种引起众所周知的代谢调整的生理压力。我们已经报道了白细胞介素 6 细胞因子家族成员心肌营养素 1 (CT-1) 的代谢特性。在这里，我们旨在分析 CT-1 在响应这些代谢变化中的作用。我们使用了不同的体内模型。此外，在进食（随意）和食物限制条件下对野生型和 CT-1 缺失小鼠进行了差异研究。我们证明了 Ct-1 是一种通过 PPARα 在肝脏中诱导的代谢基因，以响应小鼠（新生儿和食物受限的成年人）的脂质。我们发现白色脂肪组织中的 Ct-1 mRNA 表达直接涉及 PPARα 和 PPARγ。最后，CT-1 缺失小鼠中食物限制诱导的脂肪组织脂质动员受损证实了 CT-1 在禁食中的生理作用。我们的研究结果支持 CT-1 在代谢适应中的先前未被认识的生理作用，通过调节脂质代谢并有助于禁食诱导的游离脂肪酸动员。