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

Research output: Contribution to journalArticle

33 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)2644-2650
Number of pages7
JournalEndocrinology
Volume135
Issue number6
DOIs
Publication statusPublished - 1994 Jan 1
Externally publishedYes

ASJC Scopus subject areas

  • Endocrinology

Fingerprint Dive into the research topics of 'α-adrenergic receptors mediate the hypertriglyceridemia induced by endotoxin, but not tumor necrosis factor, in rats'. Together they form a unique fingerprint.

  • Cite this