LPS also induces profound endocrine and metabolic changes and our results are consistent with previously published data in pigs [27, 29, 31]. A large increase in circulating levels of cortisol (and catecholamines, not measured here) has been described and these hormonal changes can be involved in the release of the mediators of inflammation [27, 31]. It was shown previously in mice that this hypoglycaemia cannot be explained by changes in insulin concentrations that are also reduced by LPS , but it could result from the increased glycolysis in muscles and immune cells, as well as from a reduced hepatic glucose production . The increase of circulating concentration of free acids can result from the lipolytic action of catecholamines and cortisol that are massively released by LPS [11, 34] and from LPS-induced changes in hepatic and fat tissue lipid metabolism [35, 36]. A sharp increase in bilirubin concentrations was also measured at t=+4 (17.72 vs 2.14 μmol/l), reflecting the hepatic toxicity of LPS [37, 38].