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

Nonogaki, K; Moser, A H; Feingold, K R; Grunfeld, C

doi:10.1210/endo.135.6.7988454

Cited by 30Lipid metabolism and disordersLipid metabolism and biosynthesisImmune Response and Inflammation

The DOI matches its Crossref record; 19 of the 19 references it cites were found in a registry or an index.

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

Nonogaki, K, Moser, A H, Feingold, K R, Grunfeld, C·1994·Endocrinology

DOI 10.1210/endo.135.6.7988454

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Abstract

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.

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Hypertriglyceridemia in severe stress may be related to possible catecholamine induction of adipose tissue lipolysis and reduced LpL activity.
“Hypertriglyceridemia in severe stress may be related to possible catecholamine induction of adipose tissue lipolysis and reduced LpL activity (102).”
From Evaluation and Treatment of Hypertriglyceridemia: An Endocrine Society Clinical Practice Guideline (2012) · cites this paper as [102]

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Nonogaki, K., Moser, A. H., Pan, X.-M., Staprãns, I., Grünfeld, C., & Feingold, K. R. (1995) · Journal of Lipid Research · doi:10.1016/s0022-2275(20)41116-2 · Cited by 35
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Authors: Nonogaki, K., Moser, A. H., Feingold, K. R., & Grunfeld, C.
Affiliations: University of California, San Francisco (US)
ORCID: Nonogaki, K
Venue: Endocrinology
Publisher: The Endocrine Society
Published: 1994-12
Volume: 135
Issue: 6
Pages: 2644-2650
ISSN: 0013-7227 (ISSN-L)
1945-7170
DOI: 10.1210/endo.135.6.7988454
OpenAlex: W1969117650
Cited by: 30
References: 19
Citations by year: 2022: 1 · 2018: 1 · 2016: 1 · 2014: 1 · 2013: 2 · 2012: 2
FWCI: 1.89
Type: journal article
Language: en
Open access: closed
Locations: Endocrinology (publishedVersion)
PubMed (publishedVersion)
Funders: National Institute of Diabetes and Digestive and Kidney Diseases (R01DK040990, DK-40990)
Topics: Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Lipid metabolism and biosynthesis
Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
Keywords: alpha-adrenergic receptors, hypertriglyceridemia, lipopolysaccharide, endotoxin, TNF-α, catecholamines, alpha1-adrenoceptors, alpha2-adrenoceptors, hepatic triglyceride secretion, lipoprotein lipase, lipolysis, phentolamine, prazosin, yohimbine, propranolol
MeSH terms: Adrenergic alpha-Antagonists, Animals, Catecholamines, Dose-Response Relationship, Drug, Endotoxins, Lipopolysaccharides, Lipoprotein Lipase, Lipoproteins, Liver, Male, Receptors, Adrenergic, alpha, Triglycerides, Tumor Necrosis Factor-alpha, Hypertriglyceridemia, Rats, Sprague-Dawley, Rats

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

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