SOCS2 deletion protects against hepatic steatosis but worsens insulin resistance in high-fat-diet-fed mice
SOCS2 deletion protects against hepatic steatosis but worsens insulin resistance in high-fat-diet-fed mice
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DOI：
10.1096/fj.12-205583
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发表时间：
2012-08-01
期刊：
影响因子：
4.8
通讯作者：
Flores-Morales, Amilcar
中科院分区：
文献类型：
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作者：
Zadjali, Fahad;Santana-Farre, Ruyman;Flores-Morales, Amilcar
肝脏脂肪变性是生长激素(GH)缺乏患者的一个显著特征。泛素连接酶SOCS2通过抑制Janus kinase2(JAK2)信号转导和转录激活因子5b(STAT5b)轴来抑制肝脏GH信号转导。在这里，我们研究了SOCS2在饮食诱导的肝脏脂肪变性和胰岛素抵抗发展中的作用。SOCS2基因敲除(SOCS2(-/-))小鼠和野生型仔鼠在对照组和高脂饲料饲养4mo后，测定胰岛素敏感性、肝脏脂质含量和炎性细胞因子的表达。SOCS2(-/-)小鼠肝脏甘油三酯分泌增加77.6%(P
Hepatic steatosis is a prominent feature in patients with growth hormone (GH) deficiency. The ubiquitin ligase SOCS2 attenuates hepatic GH signaling by inhibiting the Janus kinase 2 (JAK2)-signal transducer and activator of transcription 5b (STAT5b) axis. Here, we investigated the role of SOCS2 in the development of diet-induced hepatic steatosis and insulin resistance. SOCS2-knockout (SOCS2(-/-)) mice and wild-type littermates were fed for 4 mo with control or high-fat diet, followed by assessment of insulin sensitivity, hepatic lipid content, and expression of inflammatory cytokines. SOCS2(-/-) mice exhibited increased hepatic TG secretion by 77.6% (P