title: Acute ethanol intoxication suppresses E. coli lipopolysaccharide enhanced glucose utilization by hepatic nonparenchymal cells.
abstract: During infection or endotoxemia, the immune system is activated and its energy needs increase. Alcohol (ETOH) intoxication on the other hand suppresses the immune system and increases susceptibility to infection. Since the liver is the primary site both for metabolism of ETOH and detoxification of bacterial lipopolysaccharides (LPS), this investigation was directed at studying the effect of acute ETOH intoxication on the LPS-induced enhancement of in vivo glucose utilization in different types of hepatic cells. Rats were given an intravenous (IV) injection of ETOH followed by a constant infusion for 7 hr to maintain blood alcohol levels at about 175 mg/dl. E. coli LPS was administered IV at 4 hr and in vivo glucose utilization by the different types of liver cells was estimated 3 hr later using the 14C-2-deoxyglucose technique. Hepatocytes (HP), Kupffer (KC), and endothelial cells (EC), as well as the sequestered polymorphonuclear leukocytes (PMN), were separated from the liver by collagenase-pronase digestion followed by centrifugal elutriation and Ficoll-Hypaque density gradient centrifugation. The number of PMN in the liver was increased several-fold 3 hr after LPS administration. The presence of ETOH did not inhibit the LPS-induced neutrophil migration into the liver. ETOH depressed the LPS-induced increase in glucose uptake in both EC and KC by 50 to 80%, respectively. It also reduced the LPS-induced increase of plasma tumor necrosis factor activity by 80%. ETOH alone did not produce any significant changes in the parameters studied.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Physiology, Louisiana State University Medical Center, New Orleans 70112.
authors.forename: N B
authors.initials: NB
authors.lastname: D'Souza
authors.forename: A P
authors.initials: AP
authors.lastname: Bautista
authors.forename: G J
authors.initials: GJ
authors.lastname: Bagby
authors.forename: C H
authors.initials: CH
authors.lastname: Lang
authors.forename: J J
authors.initials: JJ
authors.lastname: Spitzer
mesh_terms: D000435:Alcoholic Intoxication / Q000276:immunology*; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism*; D003602:Cytotoxicity, Immunologic / Q000276:immunology; D004734:Energy Metabolism / Q000502:physiology; D004926:Escherichia coli / Q000276:immunology*; D007728:Kupffer Cells / Q000276:immunology; D008070:Lipopolysaccharides / Q000276:immunology*; D008099:Liver / Q000276:immunology*; D008297:Male; D009504:Neutrophils / Q000276:immunology; D051381:Rats; D011919:Rats, Inbred Strains; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D001786:Blood Glucose; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha