<unk>  is a multi-step process resulting in the net movement of<unk>  from peripheral tissues back to the liver first via entering the lymphatic system, then the bloodstream.<unk>  from non-hepatic peripheral tissues is transferred to HDL by the ABCA1 (ATP-binding cassette<unk> er). Apolipoprotein A1 (ApoA-1), the major protein component of HDL, acts as an acceptor, and the phospholipid component of HDL acts as a sink for the mobilised<unk> . The<unk>  is converted to<unk>  esters by the enzyme LCAT (lecithin-cholesterol acyltransferase). The<unk>  esters can be transferred, with the help of CETP <unk> ester transfer protein) in exchange for triglycerides, to other lipoproteins (such as LDL and VLDL), and these lipoproteins can be taken up by secreting unesterified<unk>  into the bile or by converting<unk>  to bile acids. Adiponectin induces ABCA1-mediated<unk>  from macrophages by activation of PPAR-γ and LXRα/β. Uptake of HDL2 is mediated by hepatic lipase, a special form of lipoprotein lipase found only in the liver. Hepatic lipase activity is increased by androgens and decreased by estrogens, which may account for higher concentrations of HDL2 in women. Discoidal (Nascent) HDL: Initially, HDL is discoidal in shape because it lacks esterified<unk>  but as it keeps accumulating free<unk>  in it, the enzyme LCAT keeps esterifying the free<unk> . When the HDL molecule is<unk>  rich, its shape is changed into more spherical and it becomes less dense (HDL 2). This is carried to the liver to release all the esterified<unk>  into the liver.
Reverse cholesterol transport
Renal protein reabsorption
Renal urea handling
Renal glucose reabsorption
Renal oligopeptide reabsorption
Glyceroneogenesis
Purine metabolism
Ethanol metabolism