Cholesterol from non-hepatic peripheral tissues is transferred to HDL by the ABCA1 ( ATP-binding cassette transporter ).  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 cholesterol. The cholesterol is converted to cholesteryl esters by the enzyme LCAT ( lecithin-cholesterol acyltransferase ). The cholesteryl esters can be transferred, with the help of CETP ( cholesterylester transfer protein ) in exchange for triglycerides, to other lipoproteins (such as LDL and VLDL), and these lipoproteins can be taken up by secreting unesterified cholesterol into the bile or by converting cholesterol to bile acids .
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Andrology's July 2016 issue is devoted to the timely topic of endocrine disruption, which is suspected to be one of the factors responsible for the reported rise in the incidence of male reproductive disorders. The content of this special issue highlights some of the pertinent topics in the field that are of relevance for andrologists and researchers interested in reproductive biology and endocrinology, including female reproduction and neuroendocrinology.