Lipoteichoic acid stimulates lipolysis and hepatic triglyceride secretion in rats in vivo.

The host response to infection is frequently accompanied by changes in lipid metabolism. Previous studies have shown that endotoxin (LPS), a component of the cell wall of gram-negative bacteria, increases serum lipid levels. In this study, we demonstrate that lipoteichoic acid (LTA), a component of...

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Asıl Yazarlar: K Nonogaki, A H Moser, X M Pan, I Staprans, C Grunfeld, K R Feingold
Materyal Türü: Makale
Dil:English
Baskı/Yayın Bilgisi: Elsevier 1995-09-01
Seri Bilgileri:Journal of Lipid Research
Online Erişim:http://www.sciencedirect.com/science/article/pii/S0022227520411162
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author K Nonogaki
A H Moser
X M Pan
I Staprans
C Grunfeld
K R Feingold
author_facet K Nonogaki
A H Moser
X M Pan
I Staprans
C Grunfeld
K R Feingold
author_sort K Nonogaki
collection DOAJ
description The host response to infection is frequently accompanied by changes in lipid metabolism. Previous studies have shown that endotoxin (LPS), a component of the cell wall of gram-negative bacteria, increases serum lipid levels. In this study, we demonstrate that lipoteichoic acid (LTA), a component of the cell membrane of gram-positive bacteria, also increases serum lipid levels in rats in a dose-dependent manner (0.1-300 micrograms/200 g body weight). Serum triglyceride levels increased within 2 h after LTA administration with peak values at 4 h (2-fold increase). Serum cholesterol levels also increased but the effect was delayed occurring at 16 h and was relatively small (1.2-fold increase). LTA (10 micrograms/200 g BW) did not decrease adipose tissue lipoprotein lipase activity or the clearance of triglyceride-rich lipoproteins. Rather, the LTA-induced hypertriglyceridemia is due to an increase in hepatic triglyceride secretion. LTA stimulates both hepatic de novo fatty acid synthesis and lipolysis. The increased delivery of free fatty acids to the liver plays a major role in the LTA-induced hypertriglyceridemia. Pretreatment with phentolamine, an alpha-adrenergic receptor antagonist, and alprenolol, a beta-adrenergic receptor antagonist, or phentolamine alone significantly suppressed the hypertriglyceridemia induced by LTA. These adrenergic inhibitors had no significant effect on the increase in lipolysis. These results indicate that catecholamines are involved in mediating the LTA-induced increase in hepatic triglyceride secretion via alpha-adrenergic receptors. These changes in lipid metabolism may play an important role in the organism's response to gram-positive infection.
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spelling doaj.art-e054b623f59e49b48cb1544ae02f9e942022-12-21T22:47:13ZengElsevierJournal of Lipid Research0022-22751995-09-0136919871995Lipoteichoic acid stimulates lipolysis and hepatic triglyceride secretion in rats in vivo.K Nonogaki0A H Moser1X M Pan2I Staprans3C Grunfeld4K R Feingold5Department of Medicine, University of California, San Francisco, 94143, USA.Department of Medicine, University of California, San Francisco, 94143, USA.Department of Medicine, University of California, San Francisco, 94143, USA.Department of Medicine, University of California, San Francisco, 94143, USA.Department of Medicine, University of California, San Francisco, 94143, USA.Department of Medicine, University of California, San Francisco, 94143, USA.The host response to infection is frequently accompanied by changes in lipid metabolism. Previous studies have shown that endotoxin (LPS), a component of the cell wall of gram-negative bacteria, increases serum lipid levels. In this study, we demonstrate that lipoteichoic acid (LTA), a component of the cell membrane of gram-positive bacteria, also increases serum lipid levels in rats in a dose-dependent manner (0.1-300 micrograms/200 g body weight). Serum triglyceride levels increased within 2 h after LTA administration with peak values at 4 h (2-fold increase). Serum cholesterol levels also increased but the effect was delayed occurring at 16 h and was relatively small (1.2-fold increase). LTA (10 micrograms/200 g BW) did not decrease adipose tissue lipoprotein lipase activity or the clearance of triglyceride-rich lipoproteins. Rather, the LTA-induced hypertriglyceridemia is due to an increase in hepatic triglyceride secretion. LTA stimulates both hepatic de novo fatty acid synthesis and lipolysis. The increased delivery of free fatty acids to the liver plays a major role in the LTA-induced hypertriglyceridemia. Pretreatment with phentolamine, an alpha-adrenergic receptor antagonist, and alprenolol, a beta-adrenergic receptor antagonist, or phentolamine alone significantly suppressed the hypertriglyceridemia induced by LTA. These adrenergic inhibitors had no significant effect on the increase in lipolysis. These results indicate that catecholamines are involved in mediating the LTA-induced increase in hepatic triglyceride secretion via alpha-adrenergic receptors. These changes in lipid metabolism may play an important role in the organism's response to gram-positive infection.http://www.sciencedirect.com/science/article/pii/S0022227520411162
spellingShingle K Nonogaki
A H Moser
X M Pan
I Staprans
C Grunfeld
K R Feingold
Lipoteichoic acid stimulates lipolysis and hepatic triglyceride secretion in rats in vivo.
Journal of Lipid Research
title Lipoteichoic acid stimulates lipolysis and hepatic triglyceride secretion in rats in vivo.
title_full Lipoteichoic acid stimulates lipolysis and hepatic triglyceride secretion in rats in vivo.
title_fullStr Lipoteichoic acid stimulates lipolysis and hepatic triglyceride secretion in rats in vivo.
title_full_unstemmed Lipoteichoic acid stimulates lipolysis and hepatic triglyceride secretion in rats in vivo.
title_short Lipoteichoic acid stimulates lipolysis and hepatic triglyceride secretion in rats in vivo.
title_sort lipoteichoic acid stimulates lipolysis and hepatic triglyceride secretion in rats in vivo
url http://www.sciencedirect.com/science/article/pii/S0022227520411162
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AT xmpan lipoteichoicacidstimulateslipolysisandhepatictriglyceridesecretioninratsinvivo
AT istaprans lipoteichoicacidstimulateslipolysisandhepatictriglyceridesecretioninratsinvivo
AT cgrunfeld lipoteichoicacidstimulateslipolysisandhepatictriglyceridesecretioninratsinvivo
AT krfeingold lipoteichoicacidstimulateslipolysisandhepatictriglyceridesecretioninratsinvivo