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

• Published in: FEBS letters 1995-11, Vol.376 (1), p.65-66
• Main Authors: Mandl, J., Wall, C., Lerant, I., Falus, A., Machovich, R., Thurman, R.G.
• Format: Article
• Language: English
• Subjects: Animals; Anti-Inflammatory Agents - pharmacology; Endotoxin; Endotoxins - pharmacology; Female; Fibrin Fibrinogen Degradation Products - pharmacology; Fibrinogen degradation product; Gadolinium - pharmacology; Glucose - metabolism; Glycogen - metabolism; Glycogenolysis; Kupffer cell; Kupffer Cells - metabolism; Lactates - metabolism; Lactic Acid; Lipopolysaccharides - pharmacology; Liver; Liver - metabolism; Oxygen Consumption - drug effects; Oxygen uptake; Perfusion - methods; Rats; Rats, Sprague-Dawley
• ISSN: 0014-5793; 1873-3468
• DOI: 10.1016/0014-5793(95)01195-1

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.