SOCS2 deletion protects against hepatic steatosis but worsens insulin resistance in high-fat-diet-fed mice
Research output: Contribution to journal › Journal article › Research › peer-review
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
Original language | English |
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Journal | FASEB journal : official publication of the Federation of American Societies for Experimental Biology |
Volume | 26 |
Issue number | 8 |
Pages (from-to) | 3282-91 |
Number of pages | 10 |
DOIs | |
Publication status | Published - 2012 |
- Animals, Diet, High-Fat, Fatty Liver, Insulin Resistance, Interferon-gamma, Interleukin-6, Lipid Metabolism, Liver, Male, Mice, Mice, Knockout, NF-kappa B, Suppressor of Cytokine Signaling Proteins, Toll-Like Receptor 4, Triglycerides
Research areas
ID: 41847022