title: Very low-density lipoprotein-apoprotein CI is increased in diabetic nephropathy: comparison with apoprotein CIII.
abstract: BACKGROUND
  Recent studies have suggested that apoprotein (apo) CI in very low-density lipoprotein (VLDL) plays an important role in causing hypertriglyceridemia independent of apo CIII, which is associated with coronary heart disease (CHD). Because the incidence of CHD is increased in diabetic patients and is even higher when diabetic nephropathy is developed, we measured apo CI levels in VLDL from type 2 diabetic patients, with various degree of nephropathy, and compared the results with those for healthy controls or nondiabetic patients with chronic renal failure (CRF).
  
  
  METHODS
  This study enrolled healthy control subjects, type 2 diabetic patients with normoalbuminuria, microalbuminuria, overt proteinuria, and CRF on hemodialysis and nondiabetic hemodialysis patients. VLDL (density <1.006) was separated by ultracentrifugation. Then the apo CI, CIII, and B concentrations in VLDL were measured by enzyme-linked immunosorbent assay (ELISA).
  
  
  RESULTS
  The apo CI, CIII, and B concentrations in VLDL were respectively 3-, 2-, and 2-fold higher, respectively, in diabetic patients with overt proteinuria than in controls. Hemodialysis patients with diabetic nephropathy had levels of apo CI, CIII, and B in VLDL that were 2.6-, 2.7- and 2-fold higher, respectively, than those in controls. Nondiabetic hemodialysis patients also had a 2.7-fold higher level of VLDL apo CIII, whereas VLDL apo CI and VLDL apo B were not significantly increased. VLDL apo CI was significantly correlated with VLDL apo B independently of VLDL apo CIII level.
  
  
  CONCLUSIONS
  An increase of VLDL apo CIII is a prominent feature of dyslipidemia in CRF patients, regardless of whether they are diabetic or nondiabetic, whereas an increase of VLDL apo CI is more specific to diabetic nephropathy and is closely associated with an increase of VLDL particle numbers, a new risk factor for CHD.
authors.affiliation: First Department of Internal Medicine, Showa University School of Medicine, Tokyo, Japan. hirano@med.showa-u.ac.jp
authors.forename: Tsutomu
authors.initials: T
authors.lastname: Hirano
authors.forename: Taro
authors.initials: T
authors.lastname: Sakaue
authors.forename: Asako
authors.initials: A
authors.lastname: Misaki
authors.forename: Satoru
authors.initials: S
authors.lastname: Murayama
authors.forename: Toshihiro
authors.initials: T
authors.lastname: Takahashi
authors.forename: Kenta
authors.initials: K
authors.lastname: Okada
authors.forename: Hiroko
authors.initials: H
authors.lastname: Takeuchi
authors.forename: Gen
authors.initials: G
authors.lastname: Yoshino
authors.forename: Mitsuru
authors.initials: M
authors.lastname: Adachi
mesh_terms: D000368:Aged; D053302:Apolipoprotein C-I; D053305:Apolipoprotein C-III; D001056:Apolipoproteins C / Q000097:blood*; D015415:Biomarkers; D015243:Cholesterol, VLDL / Q000097:blood*; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000453:epidemiology; D003928:Diabetic Nephropathies / Q000097:blood* / Q000453:epidemiology*; D005260:Female; D006801:Humans; D006949:Hyperlipidemias / Q000097:blood / Q000453:epidemiology; D007676:Kidney Failure, Chronic / Q000097:blood / Q000453:epidemiology; D008297:Male; D008875:Middle Aged; D012307:Risk Factors
chemical_list: D053302:Apolipoprotein C-I; D053305:Apolipoprotein C-III; D001056:Apolipoproteins C; D015415:Biomarkers; D015243:Cholesterol, VLDL