Gadolinum chloride does not block the hypertriglyceridemia induced by LPS administration to rats.

Neyrinck A.M., Taper H.S., Delzenne NM

Unité de Pharmacocinétique, Métabolisme, Nutrition et Toxicologie, Département des Sciences Pharmaceutiques, Université Catholique de Louvain, PMNT, 73 Avenue Mounier, 1200 Bruxelles

The host response to infection and inflamation is accompanied by important disturbances in intermediary metabolism, such as hypertriglyceridemia due to an increase in very low-density lipoprotein (VLDL) secretion by the liver.  such metabolic changes can be induced by the administration of lipopolysaccharide (LPS) or TNF-alpha, the major cytokine secreted by Kupffer cells, which mediates LPS-induced lipid metabolic disorder.  The objective of the present study was to investigate the influence of GdCI³  an inhibitor of Kupffer cells phagocytic activity in the liver, does not avoid neither TNF-alpha release in the serum, not hypertriglyceridemia occuring in LPS treated rats and even promotes certain metabolic alterations due to LPS treatment.  Surprisingly, GdCI³ is able per se, in 18h-fasted rats, 1) to lead to an increase in phospholipids and HDL-cholesterol in the plasma; 2) to promote the accumulation of triglycerides in the liver tissue, an effect which could be related to an increase in phosphatidate phosphohydrolase (PAP) activity.  This later effect, since it is linked to the apparent lower activity of Kupffer cells, suggests a role of Kupffer cells in the regulation of hepatocyte metabolism.