Endotoxin and fibrinogen degradation product‐D have different actions on carbohydrate metabolism: role of Kupffer cells

FEBS Letters

Thurman, R.G.¹  Mandl, J.¹  Falus, A.²  Lerant, I.³  Machovich, R.³  Wall, C.¹ 

[1] Laboratory of Hepatobiology and Toxicology, Department of Pharmacology, University of North Carolina at Chapel Hill, NC, USA;Department of Biology, Semmelweis University of Medicine, Budapest, Hungary;2nd Department of Biochemistry, Semmelweis University of Medicine, Budapest, Hungary

关键词: Liver;    Endotoxin;    Fibrinogen degradation product;    Kupffer cell;    Glycogenolysis;    Oxygen uptake;   

DOI  :  10.1016/0014-5793(95)01195-1

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

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 GdCl₃ 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 PGE₂ and PGD₂. 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.

【 授权许可】

Unknown