Nitric oxide-induced downregulation of leptin production by 3T3-L1 adipocytes

Yuka Unno, Teruo Akuta, Yu ichiro Sakamoto, Seikoh Horiuchi, Takaaki Akaike

研究成果: Article査読

13 被引用数 (Scopus)

抄録

Leptin secreted mainly by adipocytes plays an important role in insulin sensitivity in metabolic syndrome. Inducible nitric oxide synthase (iNOS) in 3T3-L1 adipocytes is induced by lipopolysaccharide (LPS) and several proinflammatory cytokines such as tumor necrosis factor-α and interferon-γ (IFN-γ). Because the role of iNOS-derived nitric oxide (NO) in adipocyte function has not been fully clarified, the question that we addressed in the present study was whether iNOS-derived NO is involved in regulation of leptin secretion by adipocytes. Incubation of 3T3-L1 adipocytes for 12 h with a mixture of IFN-γ and LPS caused not only a 55% reduction in leptin secretion and a 52% reduction in leptin mRNA, but also significant induction of iNOS at both protein and mRNA levels. Inhibition of leptin secretion that had been induced by the IFN-γ-LPS mixture was completely nullified by NOS inhibitors such as Nω-monomethyl-l-arginine and aminoguanidine. Treatment of adipocytes with NO donors such as an NONOate and S-nitrosoglutathione produced an effect on leptin secretion similar to that of the IFN-γ-LPS mixture. It is likely therefore that NO mediates downregulation of leptin caused by the IFN-γ-LPS mixture in 3T3-L1 adipocytes, which suggests an important role for NO in adipocyte functions.

本文言語English
ページ(範囲)125-132
ページ数8
ジャーナルNitric Oxide - Biology and Chemistry
15
2
DOI
出版ステータスPublished - 2006 9

ASJC Scopus subject areas

  • Biochemistry
  • Physiology
  • Clinical Biochemistry
  • Cancer Research

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