starvation-sensing kinase adenosine monophosphate-activated protein kinase (AMPK) in H4IIEC hepatocytes. Genetic deletion of LECT2 in mice increased insulin sensitivity in the skeletal muscle. Treatment with recombinant LECT2 protein impaired insulin signaling via phosphorylation of JNK in C2C12

نویسندگان

  • Fei Lan
  • Hirofumi Misu
  • Keita Chikamoto
  • Hiroaki Takayama
  • Kensuke Mohri
  • Noboru Takata
  • Hiroto Hayashi
  • Naoto Matsuzawa-Nagata
  • Yumie Takeshita
  • Hiroyo Noda
  • Yukako Matsumoto
  • Tsuguhito Ota
  • Toru Nagano
  • Masatoshi Nakagen
  • Ken-ichi Miyamoto
  • Toru Seo
  • Kaito Iwayama
  • Seiichi Matsugo
  • Hong Tang
  • Yoshiro Saito
  • Satoshi Yamagoe
  • Shuichi Kaneko
  • Toshinari Takamura
چکیده

Recent papers have reported an association between fatty liver disease and systemic insulin resistance in humans, but the causal relationship remains unclear. The liver may contribute to muscle insulin resistance by releasing secretory proteins, termed hepatokines. Here, we demonstrate that leukocyte cell-derived chemotaxin 2 (LECT2), as an energy-sensing hepatokine, is a link between obesity and skeletal muscle insulin resistance. Circulating Page 3 of 57 Diabetes

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تاریخ انتشار 2014