title: Lipid and apolipoprotein concentrations in prenodal leg lymph of fasted humans. Associations with plasma concentrations in normal subjects, lipoprotein lipase deficiency, and LCAT deficiency.
abstract: The extent to which lipid and apolipoprotein (apo) concentrations in tissue fluids are determined by those in plasma in normal humans is not known, as all studies to date have been performed on small numbers of subjects, often with dyslipidemia or lymphedema. Therefore, we quantified lipids, apolipoproteins, high density lipoprotein (HDL) lipids, and non-HDL lipids in prenodal leg lymph from 37 fasted ambulant healthy men. Lymph contained almost no triglycerides, but had higher concentrations of free glycerol than plasma. Unesterified cholesterol (UC), cholesteryl ester (CE), phosphatidylcholine (PC), and sphingomyelin (SPM) concentrations in whole lymph were not significantly correlated with those in plasma. HDL lipids, but not non-HDL lipids, were directly related to those in plasma. Lymph HDLs were enriched in UC. However, as the HDL cholesterol/non-HDL cholesterol ratio in lymph exceeded that in plasma, whole lymph nevertheless had a lower UC/CE ratio than plasma. Lymph also had a significantly higher SPM/PC ratio. The lymph/plasma (L/P) ratios of apolipoproteins were as follows: A-IV > A-I and A-II > C-III and E > B. Comparison with the L/P ratios of seven nonlipoprotein proteins suggested that apoA-IV was predominantly lipid free. Concentrations of apolipoproteins A-II, A-IV, C-III, and E in lymph, but not of apolipoproteins A-I or B, were positively correlated with those in plasma. The L/P ratios of apolipoproteins B, C-III, and E in two subjects with lipoprotein lipase (LPL) deficiency, and of apolipoproteins A-I and A-IV in a subject with lecithin:cholesterol acyltransferase (LCAT) deficiency, were low relative to those in normal subjects. Thus, the concentrations of lipids, apolipoproteins, and lipoproteins in human tissue fluid are determined only in part by their concentrations in plasma. Other factors, including the actions of LPL and LCAT, are at least as important.
authors.affiliation: Department of Cardiovascular Biochemistry, St. Bartholomew's and the Royal London School of Medicine and Dentistry, London EC1M 6BQ, UK.
authors.forename: M N
authors.initials: MN
authors.lastname: Nanjee
authors.forename: C J
authors.initials: CJ
authors.lastname: Cooke
authors.forename: W L
authors.initials: WL
authors.lastname: Olszewski
authors.forename: N E
authors.initials: NE
authors.lastname: Miller
mesh_terms: D000328:Adult; D000368:Aged; D053305:Apolipoprotein C-III; D001053:Apolipoproteins / Q000032:analysis* / Q000097:blood; D001054:Apolipoproteins A / Q000032:analysis / Q000097:blood; D001055:Apolipoproteins B / Q000032:analysis / Q000097:blood; D001056:Apolipoproteins C / Q000032:analysis / Q000097:blood; D001057:Apolipoproteins E / Q000032:analysis / Q000097:blood; D002784:Cholesterol / Q000032:analysis / Q000097:blood; D008076:Cholesterol, HDL / Q000032:analysis / Q000097:blood; D005260:Female; D005990:Glycerol / Q000032:analysis / Q000097:blood; D006801:Humans; D007866:Leg; D008055:Lipids / Q000032:analysis* / Q000097:blood; D008071:Lipoprotein Lipase / Q000172:deficiency*; D008074:Lipoproteins / Q000032:analysis / Q000097:blood; D008075:Lipoproteins, HDL / Q000032:analysis / Q000097:blood; D008196:Lymph / Q000737:chemistry*; D008297:Male; D008875:Middle Aged; D009154:Mutation; D007862:Phosphatidylcholine-Sterol O-Acyltransferase / Q000235:genetics*; D014280:Triglycerides / Q000032:analysis / Q000097:blood
chemical_list: D053305:Apolipoprotein C-III; D001053:Apolipoproteins; D001054:Apolipoproteins A; D001055:Apolipoproteins B; D001056:Apolipoproteins C; D001057:Apolipoproteins E; D008076:Cholesterol, HDL; D008055:Lipids; D008074:Lipoproteins; D008075:Lipoproteins, HDL; D014280:Triglycerides; D002784:Cholesterol; D007862:Phosphatidylcholine-Sterol O-Acyltransferase; D008071:Lipoprotein Lipase; D005990:Glycerol