**1. Introduction**

198 Dyslipidemia - From Prevention to Treatment

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thickening and vascular reactivity in humans. Elevated high-density lipoprotein levels ameliorate abnormal vasoconstriction in early atherosclerosis: Circulation, v. Gram-negative sepsis is an increasingly clinical syndrome triggered by exposure to bacterial lipopolysaccharide (LPS) or endotoxin. It is associated with a plethora of physiological and biochemical changes, known as acute-phase response (APR), including disturbances in serum lipid and lipoprotein levels (Khovidhunkit et al., 2004). Within the blood, LPS is extracted by the acute phase reactant LPS-binding protein (LBP) and transferred to CD14 receptor on monocytes and macrophages. The CD14 associates with Toll like receptor 4, myeloid differentiation-2 and other proteins forming a receptor cluster that leads to LPSinduced activation (Triantafilou & Triantafilou, 2005), resulting in the release of soluble mediators, such as proinflammatory cytokines.

Kupffer cells (KC), the resident machrophages in the liver, secrete cytokines, particularly tumor necrosis factor α (TNF-α) and the interleukins (IL) IL-6 and IL-1β, that act as paracrine factors on neighboring hepatocytes and promote many of the metabolic changes that accompany the acute-phase response. One of the most striking changes associated to sepsis is the accumulation of triglycerides (TG) within very low density lipoprotein (VLDL) in the plasma, partly ascribed to an increased hepatic VLDL production and a decreased peripheral metabolism driven by pro-inflammatory cytokines. These metabolic alterations, clinically termed as the "lipemia of sepsis", have been postulated to be components of the innate defensive reaction against infection (Harris et al., 2000).

In this chapter we summarize the actual knowledge on sepsis induced alterations in VLDL metabolism, lipids and apoB availability and the involvement of inflammatory mediators.
