LIF and CNTF, which share the gp130 transduction system, stimulate hepatic lipid metabolism in rats

Katsunori Nonogaki, Xian Mang Pan, Arthur H. Moser, Judy Shigenaga, Ilona Staprans, Nobuo Sakamoto, Carl Grunfeld, Kenneth R. Feingold

研究成果: Article査読

19 被引用数 (Scopus)

抄録

We determined the effects of leukemia inhibitory factor (LIF) and ciliary neurotrophic factor (CNTF) on lipid metabolism in intact rats. Administration of LIF and CNTF increased serum triglycerides in a dose- dependent manner with peak values at 2h. The effects of LIF and CNTF on serum cholesterol were very small, and serum glucose was unaffected. Both LIF and CNTF stimulated hepatic triglyceride secretion, hepatic de novo fatty acid synthesis, and lipolysis. Pretreatment with phenylisopropyl adenosine, which inhibits lipolysis, partially inhibited LIF- and CNTF-induced hypertriglyceridemia. Interleukin-4, which inhibits cytokine-induced hepatic fatty acid synthesis, also partially inhibited LIF- and CNTF-induced hypertriglyceridemia. These results indicate that both lipolysis and de novo fatty acid synthesis play a role in providing fatty acids for the increase in hepatic triglyceride secretion. Neither indomethacin nor adrenergic receptor antagonists affected the hypertriglyceridemia. The combination of LIF plus CNTF showed no additive effects consistent with the action of both cytokines through the gp130 transduction system. Thus LIF and CNTF have similar effects on lipid metabolism; they join a growing list of cytokines that stimulate hepatic triglyceride secretion and may mediate the changes in lipid metabolism that accompany the acute phase response.

本文言語English
ページ(範囲)E521-E528
ジャーナルAmerican Journal of Physiology - Endocrinology and Metabolism
271
3 34-3
DOI
出版ステータスPublished - 1996 9
外部発表はい

ASJC Scopus subject areas

  • 内分泌学、糖尿病および代謝内科学
  • 生理学
  • 生理学(医学)

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