Hypertriglyceridemia, Metabolic Syndrome, and Cardiovascular Disease in HIV-Infected Patients: Effects of Antiretroviral Therapy and Adipose Tissue Distribution

Figure 2

Pathogenesis of CART-related hyperlipidemia. Several factors contribute to hyperlipidemia in HIV-infected patients. PIs suppress the breakdown of the nuclear form of SREBP-1, as well as the proteasomal degradation of nascent apoB in the liver, leading to increased VLDL secretion (1). In the postprandial phase due to limited LPL availability, competition at the level of LPL will occur resulting in accumulation of TRL. This competition is most likely when fasting hypertriglyceridemia is present. In addition, impaired disposal of TRL is likely due to a defect in LPL activity (2) and delayed removal of remnant particles by liver receptors (3). Impaired FFA storage capacity (4) may lead to increased flux of circulating lipids (5) and upregulate hepatic VLDL production in patients with lipodystrophy.