title: Reduced apolipoprotein glycosylation in patients with the metabolic syndrome.
abstract: OBJECTIVE
  The purpose of this study was to compare the apolipoprotein composition of the three major lipoprotein classes in patients with metabolic syndrome to healthy controls.
  
  
  METHODS
  Very low density (VLDL), intermediate/low density (IDL/LDL, hereafter LDL), and high density lipoproteins (HDL) fractions were isolated from plasma of 56 metabolic syndrome subjects and from 14 age-sex matched healthy volunteers. The apolipoprotein content of fractions was analyzed by one-dimensional (1D) gel electrophoresis with confirmation by a combination of mass spectrometry and biochemical assays.
  
  
  RESULTS
  Metabolic syndrome patients differed from healthy controls in the following ways: (1) total plasma--apoA1 was lower, whereas apoB, apoC2, apoC3, and apoE were higher; (2) VLDL--apoB, apoC3, and apoE were increased; (3) LDL--apoC3 was increased, (4) HDL--associated constitutive serum amyloid A protein (SAA4) was reduced (p<0.05 vs. controls for all). In patients with metabolic syndrome, the most extensively glycosylated (di-sialylated) isoform of apoC3 was reduced in VLDL, LDL, and HDL fractions by 17%, 30%, and 25%, respectively (p<0.01 vs. controls for all). Similarly, the glycosylated isoform of apoE was reduced in VLDL, LDL, and HDL fractions by 15%, 26%, and 37% (p<0.01 vs. controls for all). Finally, glycosylated isoform of SAA4 in HDL fraction was 42% lower in patients with metabolic syndrome compared with controls (p<0.001).
  
  
  CONCLUSIONS
  Patients with metabolic syndrome displayed several changes in plasma apolipoprotein composition consistent with hypertriglyceridemia and low HDL cholesterol levels. Reduced glycosylation of apoC3, apoE and SAA4 are novel findings, the pathophysiological consequences of which remain to be determined.
authors.affiliation: Cardiovascular Health Research Center, Sanford Research USD, Sioux Falls, South Dakota, United States of America.
authors.forename: Olga V
authors.initials: OV
authors.lastname: Savinova
authors.affiliation: Cardiovascular Health Research Center, Sanford Research USD, Sioux Falls, South Dakota, United States of America.
authors.forename: Kristi
authors.initials: K
authors.lastname: Fillaus
authors.affiliation: Department of Chemistry and Biochemistry, South Dakota State University, Brookings, South Dakota, United States of America.
authors.forename: Linhong
authors.initials: L
authors.lastname: Jing
authors.affiliation: Department of Internal Medicine, Sanford School of Medicine, University of South Dakota, Vermillion, South Dakota, United States of America.
authors.forename: William S
authors.initials: WS
authors.lastname: Harris
authors.affiliation: Cardiovascular Health Research Center, Sanford Research USD, Sioux Falls, South Dakota, United States of America; Department of Internal Medicine, Sanford School of Medicine, University of South Dakota, Vermillion, South Dakota, United States of America.
authors.forename: Gregory C
authors.initials: GC
authors.lastname: Shearer
mesh_terms: D000328:Adult; D001053:Apolipoproteins / Q000097:blood* / Q000737:chemistry / Q000145:classification; D016022:Case-Control Studies; D005260:Female; D006031:Glycosylation; D006801:Humans; D008075:Lipoproteins, HDL / Q000097:blood / Q000737:chemistry; D053419:Lipoproteins, IDL / Q000097:blood / Q000737:chemistry; D008077:Lipoproteins, LDL / Q000097:blood / Q000737:chemistry; D008079:Lipoproteins, VLDL / Q000097:blood / Q000737:chemistry; D008297:Male; D024821:Metabolic Syndrome / Q000097:blood*; D008875:Middle Aged; D000685:Serum Amyloid A Protein / Q000737:chemistry / Q000378:metabolism
chemical_list: D001053:Apolipoproteins; D008075:Lipoproteins, HDL; D053419:Lipoproteins, IDL; D008077:Lipoproteins, LDL; D008079:Lipoproteins, VLDL; C094771:SAA4 protein, human; D000685:Serum Amyloid A Protein