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Transplantation [http://www.selleckchem.com/products/i-bet151-gsk1210151a.html I-BET151 datasheet] of ABCA1- or ABCG1-deficient bone marrow resulted in 45% and 23% decreases of 27OHC plasma levels as well as in significantly decreased 27OHC/cholesterol ratios (p?[http://www.selleckchem.com/products/mk-4827-niraparib-tosylate.html Selleckchem MK-4827] of 27OHC. The very low plasma and lipoprotein concentrations of 27OHC, the significant correlations between 27OHC and cholesterol concentrations in plasma and lipoproteins [9] as well as the higher water-solubility of 27OHC compared to cholesterol [3] raised the question whether 27OHC is [http://www.selleckchem.com/products/ly2109761.html selleck] passively equilibrated among the various lipoprotein classes or specifically metabolized in plasma similar to cholesterol, that is by established transporters, enzymes, lipid transfer proteins and receptors. Some general support for the latter assumption could already be derived from the enrichment of 27OHC relative to cholesterol in HDL (on average 47?��?7% of plasma 27OHC instead of 33?��?6% plasma cholesterol) [9] and from the 10% higher percentages of 27OHC-esters relative to cholesterylesters in plasma, HDL and LDL [9]. We here further explored this question by analysing 27OHC concentrations in plasma as well as HDL- and nonHDL-fractions of patients and mice with distinct monogenic disorders of HDL metabolism. In the present study correlations between 27OHC and cholesterol concentrations in plasma and HDL were similar or even stronger than those reported by us previously, namely 0.59 instead of 0.54 in total plasma, and 0.64 instead of 0.34 in HDL (Fig. 1 and [9]). Independently of the metabolic or genetic origin, differences in HDL cholesterol appear to explain up to 40% of the variation in HDL-27OHC levels. As a consequence, functionally relevant mutations in apoA-I, ABCA1 and LCAT that decrease HDL-cholesterol were associated with reduced concentrations of 27OHC in HDL.