PMID- 7988454
OWN - NLM
STAT- MEDLINE
DCOM- 19950106
LR  - 20071114
IS  - 0013-7227 (Print)
IS  - 0013-7227 (Linking)
VI  - 135
IP  - 6
DP  - 1994 Dec
TI  - Alpha-adrenergic receptors mediate the hypertriglyceridemia induced by endotoxin, 
      but not tumor necrosis factor, in rats.
PG  - 2644-50
AB  - We assessed the role of catecholamines in mediating the hypertriglyceridemia 
      induced by lipopolysaccharide (LPS) or tumor necrosis factor-alpha (TNF alpha) in 
      rats by employing specific adrenoreceptor antagonists. Pretreatment with 
      phentolamine, an alpha-antagonist, but not propranolol, a beta-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 alpha 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 alpha 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 alpha. In summary, these findings suggest that catecholamines via 
      alpha-adrenergic, but not beta-adrenergic, receptors are mediators of the 
      hypertriglyceridemia induced by either low or high dose LPS in rats. alpha 
      1-Adrenergic receptors are involved in mediating the increased hepatic 
      triglyceride secretion induced by low dose LPS, whereas alpha 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 alpha in rats.
FAU - Nonogaki, K
AU  - Nonogaki K
AD  - Department of Medicine, University of California, San Francisco 94143.
FAU - Moser, A H
AU  - Moser AH
FAU - Feingold, K R
AU  - Feingold KR
FAU - Grunfeld, C
AU  - Grunfeld C
LA  - eng
GR  - DK-40990/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Endocrinology
JT  - Endocrinology
JID - 0375040
RN  - 0 (Adrenergic alpha-Antagonists)
RN  - 0 (Catecholamines)
RN  - 0 (Endotoxins)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Lipoproteins)
RN  - 0 (Receptors, Adrenergic, alpha)
RN  - 0 (Triglycerides)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - EC 3.1.1.34 (Lipoprotein Lipase)
SB  - IM
MH  - Adrenergic alpha-Antagonists/pharmacology
MH  - Animals
MH  - Catecholamines/physiology
MH  - Dose-Response Relationship, Drug
MH  - *Endotoxins
MH  - Hypertriglyceridemia/blood/*chemically induced
MH  - Lipopolysaccharides/pharmacology
MH  - Lipoprotein Lipase/blood
MH  - Lipoproteins/metabolism
MH  - Liver/metabolism
MH  - Male
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptors, Adrenergic, alpha/*physiology
MH  - Triglycerides/metabolism
MH  - *Tumor Necrosis Factor-alpha
EDAT- 1994/12/01 00:00
MHDA- 1994/12/01 00:01
CRDT- 1994/12/01 00:00
PHST- 1994/12/01 00:00 [pubmed]
PHST- 1994/12/01 00:01 [medline]
PHST- 1994/12/01 00:00 [entrez]
AID - 10.1210/endo.135.6.7988454 [doi]
PST - ppublish
SO  - Endocrinology. 1994 Dec;135(6):2644-50. doi: 10.1210/endo.135.6.7988454.