Summary
Lipopolysaccharide (LPS), the active principle of certain endotoxins, protein-free perfused in rat hearts leads in 3 h to a considerable loss of lipoprotein lipase (LPL) activity. In the presence of albumin LPS has virtually no effect. Tumor necrosis factor (TNF) added instead of LPS had no effects on LPL activity during 3 hin vitro perfusion.
LPS injected into rats intravenously leads within 3 h to severe toxic phenomena amongst which increased capillary permeability. This was visualized as increased rate of interstitial fluid formation in Langendorff hearts mounted 3 h after rats had been treated with LPS. LPL activity did not decline in 3 h lasting endotoxemia. Six hours after LPS injection, however, cardiac LPL activity was considerably lowered, although immunoblotting and immunohistochemistry still showed LPL protein to be present. These date indicate the presence of a considerable pool of inactive LPL protein in addition to active LPL, that can be released in the presence of heparin. The LPL activity is lowered by LPS injection after a lag phase of at least 3 h, while capillary endothelial cells are influenced more rapidly. The relatively late expression of TNF toxicity in cardiomyocytes of the intact heart is discussed.
This is a preview of subscription content, log in via an institution to check access.
Similar content being viewed by others
References
Beutler B, Mahoney J, Le Trang N, Pekala P, Cerami A: Purification of cachectin, a lipoprotein lipase suppressing hormone secreted by endotoxin induced RAW 264.7 cells. J Exp Med 161:984–995, 1985
Pekala PH, Kawakami M, Angus CW, Lane MD, Cerami A: Selective inhibition of synthesis of enzymes for de novo fatty acid biosynthesis by an endotoxin-induced mediator from exudate cells. Proc Natl Acad Sci USA 80:2743–2747, 1983
Price SR, Olivecrona T, Pekala PH: Regulation of lipoprotein lipase synthesis by recombinant tumor necrosis factor — the primary regulatory role of the hormone in 3T3-Li adipocytes. Arch Biochem Biophys 251:738–746, 1986
Hülsmann WC, Lamers JMJ, Stam H, Breeman WAP: Calcium overload in endotoxemia. Life Sci 10:1009–1014, 1981
Bagby GJ, Spitzer JA: Lipoprotein lipase activity in rat heart and adipose tissue during endotoxic shock. Am J Physiol 238:H325-H330, 1980
Robinson DS: The function of the plasma triglycerides in fatty acid transport. Comp Biochem 18:51–116, 1970
Le J, Vilćek J: Tumor necrosis factors and Interleukin-1: cytokines with multiple overlapping biological activities. Lab Invest 56:234–248, 1987
Ryan US, Ryan JW, Crutchley DJ: Pulmonary endothelial surface. Fed Proc 44:2603–2609, 1985
De Deckere EAM, Ten Hoor F: A modified Langendorff technique for metabolic investigations. Pflügers Arch 370:102–105, 1977
Nilsson-Ehle P, Schotz MC: A stable, radioactive substrate emulsion for assay of lipoprotein lipase. J Lipid Res 17:536–541, 1976
Hülsmann WC, Dubelaar ML: Lipoprotein lipases and stresshormones; studies with glucocorticoids and cholera toxin. Biochim Biophys Acta 875:69–75, 1986
Persoon NLM, Sips HJ, Hulsmann WC, Jansen H: Monoclonal antibodies against salt-resistant rat liver lipase. Cross-reactivity with lipases from rat adrenals and ovaries. Biochim Biophys Acta 875:286–292, 1986
Stam H, Hülsmann WC: Effects of hormones, amino acids and specific inhibitors on rat heart heparin-releasable lipoprotein lipase and tissue neutral lipase activities during long-term perfusion. Biochim Biophys Acta 794:72–82, 1984
Persoon NLM, Hulsmann WC, Jansen H: Localization of salt-resistant heparin-releasable lipase in the rat liver, adrenal and ovary. Eur J Cell Biol 41:134–137, 1986
Chen RF: Removal of fatty acids from serum albumin by charcoal treatment. J Biol Chem 242:173–181, 1967
Friedman G, Chajek-Shaul T, Etienne J, Stein O, Stein Y Characterization of lipoprotein lipase in the functional pool of rat heart by immunoblotting. Biochim Biophys Acta 875:397–399, 1982
Hulsmann WC, Stam H, Breeman WAP: On the neutral lipase in rat heart. Biochem Biophys Res Commun 108:371–378, 1982
Philipson KD, Langer GA, Rich TL: Charged amphiphiles regulate heart contractility and sarcolemma-Ca2+ interactions. Am J Physiol 248:H147-H150, 1985
Hülsmann WC: Coronary vasodilation by fatty acids. Basic Res Cardiol 71:179–191, 1976
Stam H, Hulsmann WC: The relation between fatty acid mobilization and contractility in the isolated, perfused rat heart. Biochem Biophys Res Commun 82:609–614, 1978
Osborne JC, Bengtsson-Olivecrona G, Lee NS, Olivecrona T: Studies on the inactivation of lipoprotein lipase: role of dimer to monomer dissociation. Biochemistry 2406–5611, 1985
Semb H, Peterson J, Tavernier J, Olivecrona T. Multiple effects of tumor necrosis factor on lipoprotein lipase in vivo. J Biol Chem 262:8390–8394, 1987
Kawakami M, Cerami A: Studies of endotoxin-induced decrease in lipoprotein lipase activity. J Exp Med 154:631–639, 1981
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Hülsmann, W.C., Dubelaar, ML., De Wit, L.E.A. et al. Cardiac lipoprotein lipase: effects of lipopolysaccharide and tumor necrosis factor. Mol Cell Biochem 79, 137–145 (1988). https://doi.org/10.1007/BF02424556
Received:
Accepted:
Issue Date:
DOI: https://doi.org/10.1007/BF02424556