title: Cell surface expression of LDL receptor is decreased in type 2 diabetic patients and is normalized by insulin therapy.
abstract: OBJECTIVE
  In type 2 diabetic patients with poor metabolic control, kinetic studies have demonstrated that LDL fractional catabolic rate (FCR) is slowed down, whereas it is normalized on insulin therapy. This study was designed to analyze whether variations in the expression of LDL receptors at the cell surface could explain the results observed in kinetic studies.
  
  
  METHODS
  LDL receptors were quantified at the surface of mononuclear cells in fresh fasting blood samples by a flow cytometry method in 21 control subjects and 21 type 2 diabetic patients before and 3 months after the introduction of insulin therapy and concomitant removal of oral antidiabetic drugs.
  
  
  RESULTS
  Before insulin treatment, monocyte LDL receptor expression was reduced by 41% (6,439 +/- 2,310 vs. 10,846 +/- 2,764 receptors per monocyte, P < 0.001) in type 2 diabetic patients compared with control subjects. It increased by 57% after 3 months of insulin therapy (10,096 +/- 5,657 vs. 6,439 +/- 2,310, P < 0.01) and was similar to that observed in control subjects.
  
  
  CONCLUSIONS
  Our results suggest that insulin plays an important role in the in vivo expression of LDL receptors. Moreover, modulations in the expression of LDL receptors in type 2 diabetic patients either with poor metabolic control or on insulin therapy are likely to contribute to the variations of LDL FCR demonstrated by kinetic studies under those circumstances.
authors.affiliation: Unity INSERM 498, Hôpital du Bocage, Dijon Cédex, France. laurence.duvillard@chu-dijon.fr
authors.forename: Laurence
authors.initials: L
authors.lastname: Duvillard
authors.forename: Emmanuel
authors.initials: E
authors.lastname: Florentin
authors.forename: Gérard
authors.initials: G
authors.lastname: Lizard
authors.forename: Jean-Michel
authors.initials: JM
authors.lastname: Petit
authors.forename: Françoise
authors.initials: F
authors.lastname: Galland
authors.forename: Serge
authors.initials: S
authors.lastname: Monier
authors.forename: Philippe
authors.initials: P
authors.lastname: Gambert
authors.forename: Bruno
authors.initials: B
authors.lastname: Vergès
mesh_terms: D000284:Administration, Oral; D000368:Aged; D001786:Blood Glucose / Q000378:metabolism; D002462:Cell Membrane / Q000378:metabolism; D002784:Cholesterol / Q000097:blood; D003924:Diabetes Mellitus, Type 2 / Q000188:drug therapy* / Q000378:metabolism*; D005260:Female; D006801:Humans; D007004:Hypoglycemic Agents / Q000008:administration & dosage / Q000627:therapeutic use; D007328:Insulin / Q000097:blood / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000378:metabolism; D011973:Receptors, LDL / Q000097:blood*; D012016:Reference Values; D017211:Treatment Failure; D014280:Triglycerides / Q000097:blood
chemical_list: D001786:Blood Glucose; D007004:Hypoglycemic Agents; D007328:Insulin; D011973:Receptors, LDL; D014280:Triglycerides; D002784:Cholesterol