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Endotoxin and fibrinogen degradation product‐D have different actions on carbohydrate metabolism: role of Kupffer cells
Author(s) -
Mandl J.,
Wall C.,
Lerant I.,
Falus A.,
Machovich R.,
Thurman R.G.
Publication year - 1995
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(95)01195-1
Subject(s) - glycogenolysis , glycogen , lipopolysaccharide , kupffer cell , chemistry , oxygen , stimulation , medicine , endocrinology , fibrinogen , metabolism , biochemistry , biology , organic chemistry
The effect of endotoxin‐derived lipopolysaccharide (LPS) and fibrinogen degradation product D (FDPD) on oxygen consumption and glycogenolysis in the perfused rat liver was investigated. 1. Infusion of LPS (100 μg/ml) or FDPD (7 μg/ml) caused a rapid stimulation of oxygen uptake by the perfused liver of 10–12 μmol/g/h. 2. LPS also caused a transient increase in glucose and lactate release into the perfusion medium from endogenous glycogen; however, FDPD was without effect. 3. Destruction of Kupffer cells by GdCl 3 pretreatment blocked the effects of LPS and FDPD on oxygen uptake and glycogenolysis. Further, LPS and FDPD had no effect on oxygen consumption by isolated hepatocytes. Therefore, it is concluded that Kupffer cells are involved in the increase of hepatic oxygen consumption and carbohydrate release caused by LPS, most likely via release of PGE 2 and PGD 2 . Since FDPD increased oxygen but not carbohydrate release, it is concluded that it acts via stimulating the release of mediators distinct from those released following LPS infusion.