This Article Full Text Full Text (PDF) Purchase Article View Shopping Cart Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Liao, W. Articles by Angelin, B. Search for Related Content PubMed PubMed Citation Articles by Liao, W. Articles by Angelin, B.

Novel Effects of Histamine on Lipoprotein Metabolism: Suppression of Hepatic Low Density Lipoprotein Receptor Expression and Reduction of Plasma High Density Lipoprotein Cholesterol in the Rat¹

Molecular Nutrition Unit, Center for Nutrition and Toxicology, NOVUM, and the Metabolism Unit, Center for Metabolism and Endocrinology, Department of Medicine, Karolinska Institute, Huddinge University Hospital, Huddinge, Sweden

Address all correspondence and requests for reprints to: Wei Liao, M.D., Ph.D., Department of Cell Biology, Baylor College of Medicine, 1 Baylor Plaza, Houston, Texas 77030.

Histamine has been shown to be involved in atherosclerosis and coronary heart disease. Little information is available regarding the effects of histamine on lipoprotein metabolism. In the current study, we investigated the effects of histamine on the expression of hepatic low density lipoprotein (LDL) receptors and on plasma lipoproteins in the rat. Injection of compound 48/80 (C48/80, a histamine releaser) or histamine reduced hepatic LDL receptor expression, but not LDL receptor messenger RNA levels. Oral administration of polymyxin B (an antiendotoxin antibiotic and a histamine releaser) before the injection of C48/80 or histamine did not attenuate their effects. Polymyxin B itself had effects similar to those of C48/80 and histamine on LDL receptors. These results suggest that the effects of histamine are not mediated by the induction of gut-derived endotoxemia. Histamine H2 agonists (dimaprit and impromidine), but not H1 agonists (2-methylhistamine and 2-thiazolylethylamine), also reduced hepatic LDL receptor expression. The suppressive effect of C48/80 on hepatic LDL receptor expression was not attenuated by either the H1 antagonist (chlorpheniramine) or the H2 antagonist (cimetidine). Administration of C48/80 also reduced plasma high density lipoprotein (HDL) cholesterol. The H1 antagonist (chlorpheniramine), but not the H2 antagonist (cimetidine), almost completely reversed the effect of C48/80 on plasma HDL cholesterol. In conclusion, histamine suppresses hepatic LDL receptor expression via a non-H1 receptor-mediated pathway, and histamine reduces plasma HDL cholesterol via an H1 receptor-mediated pathway.

This article has been cited by other articles:

				K. N. Maxwell, E. A. Fisher, and J. L. Breslow Overexpression of PCSK9 accelerates the degradation of the LDLR in a post-endoplasmic reticulum compartment PNAS, February 8, 2005; 102(6): 2069 - 2074. [Abstract] [Full Text] [PDF]

				S. Tanaka, K.-i. Nemoto, E. Yamamura, and A. Ichikawa Intracellular Localization of the 74- and 53-kDa Forms of L-Histidine Decarboxylase in a Rat Basophilic/Mast Cell Line, RBL-2H3 J. Biol. Chem., April 3, 1998; 273(14): 8177 - 8182. [Abstract] [Full Text] [PDF]