α-adrenergic receptors mediate the hypertriglyceridemia induced by endotoxin, but not tumor necrosis factor, in rats

Katsunori Nonogaki, Arthur H. Moser, Kenneth R. Feingold, Carl Grunfeld

研究成果: Article査読

33 被引用数 (Scopus)

抄録

We assessed the role of catecholamines in mediating the hypertriglyceridemia induced by lipopolysaccharide (LPS) or tumor necrosis factor-α (TNF α) in rats by employing specific adrenoreceptor antagonists. Pretreatment with phentolamine, an α-antagonist, but not propranolol, a β-antagonist, suppressed the hypertriglyceridemia induced by either low dose LPS (100 ng/100 g BW) or high dose LPS (50 micrograms/100 g BW). Prazosin, an α 1-selective antagonist, significantly suppressed the low dose LPS-induced hypertriglyceridemia by inhibiting hepatic triglyceride secretion, but did not affect the increase in lipolysis. In contrast, yohimbine, an α 2-selective antagonist, partially suppressed the high dose LPS-induced hypertriglyceridemia by inhibiting the decrease in postheparin lipoprotein lipase activity. Treatment with phentolamine and propranolol did not affect the hypertriglyceridemia induced by TNF α. In summary, these findings suggest that catecholamines via α-adrenergic, but not β-adrenergic, receptors are mediators of the hypertriglyceridemia induced by either low or high dose LPS in rats. α 1-Adrenergic receptors are involved in mediating the increased hepatic triglyceride secretion induced by low dose LPS, whereas α 2-adrenergic receptors are involved in mediating the decrease in lipoprotein lipase activity induced by high dose LPS. The hypertriglyceridemia induced by either low or high dose LPS may be regulated by a mechanism unrelated to TNF α in rats.

本文言語English
ページ(範囲)2644-2650
ページ数7
ジャーナルEndocrinology
135
6
DOI
出版ステータスPublished - 1994 12
外部発表はい

ASJC Scopus subject areas

  • Endocrinology

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