Cytokine-induced alterations in lipid and lipoprotein metabolism often accompany infection and inflammation. Inflammatory cytokines are elevated and play a pathogenic role in disorders such as diabetes, obesity, the metabolic syndrome, and CVD. Many of these disorders present lipid metabolism abnormalities that are similar to those that occur during infection and inflammation.
The characteristic lipid metabolism disturbances found during inflammation are increased triglyceride concentrations and decreased HDL cholesterol levels. Inflammation and atherogenic dyslipidemia may be linked by the fact that TNF-α and IL-6 stimulate lipolysis, increasing FFA flux to the liver (Figure 2). This increase in FFA induces hepatic triglyceride synthesis (by increasing hepatic de novo fatty acid synthesis or the reesterification of fatty acids derived from peripheral lipolysis) and increases liver VLDL secretion, both of which increase hepatic triglyceride production and secretion causing hypertriglyceridemia (34). TNF-α and IL-6 also suppress lipoprotein lipase synthesis in adipose tissue, which could contribute to the hypertriglyceridemia and low HDL cholesterol concentrations observed in individuals with intra-abdominal obesity (35). With respect to low HDL cholesterol, inflammation and cytokines can modify the size, composition, and function of HDL particles in several ways. Inflammation-related changes to HDL particles not only lower HDL cholesterol levels but also alter the anti-oxidant properties of HDL. It is thought that the lowering of HDL cholesterol levels during inflammation is due to a reduction in cholesterol uptake by cells and an increase in their catabolism (36).

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