SOCS2 deletion protects against hepatic steatosis but worsens insulin resistance in high-fat-diet-fed mice

Research output: Contribution to journalJournal articleResearchpeer-review

  • Fahad Zadjali
  • Ruyman Santana-Farre
  • Mattias Vesterlund
  • Berit Carow
  • Mercedes Mirecki-Garrido
  • Irene Hernandez-Hernandez
  • Malin Flodström-Tullberg
  • Paolo Parini
  • Martin Rottenberg
  • Gunnar Norstedt
  • Leandro Fernandez-Perez
  • Amilcar Flores Morales
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 languageEnglish
JournalFASEB journal : official publication of the Federation of American Societies for Experimental Biology
Issue number8
Pages (from-to)3282-91
Number of pages10
Publication statusPublished - 2012

    Research areas

  • 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

ID: 41847022