title: Insulin sensitivity and lipid metabolism in human CD36 deficiency.
abstract: OBJECTIVE
  CD36 has been proposed as a fatty acid translocase and a receptor for HDL and oxidized LDL. The association between CD36 deficiency and insulin resistance remains controversial. We investigated glucose and lipid metabolism in human CD36 deficiency.
  
  
  METHODS
  A total of 61 type I CD36-deficient patients and 25 control subjects were examined. Diabetes was defined as fasting glucose level > or =7 mmol/l or use of hypoglycemic agents. A homeostasis model assessment (HOMA) index was evaluated in patients without diabetes. Insulin resistance was defined as a HOMA index > or =1.73 (sensitivity 64.3%, specificity 78.9%; J Japan Diab Soc, 2000).
  
  
  RESULTS
  Diabetes was identified in 12 (20%) of the 61 CD36-deficient patients. Fasting glucose, HbA(1c), and total cholesterol levels in the diabetic CD36-deficient patients were significantly higher than in the control subjects and the nondiabetic CD36-deficient patients. Regardless of diabetes, HDL cholesterol concentrations in the CD36-deficient patients were significantly higher than in the control subjects. The nondiabetic CD36-deficient patients had higher triglyceride concentrations than the control subjects, and triglyceride concentrations were higher in the diabetic CD36-deficient patients than in the nondiabetic CD36-deficient patients. The prevalence of insulin resistance in the nondiabetic CD36-deficient patients was similar to that in the control subjects.
  
  
  CONCLUSIONS
  Human CD36 deficiency is not necessarily responsible for insulin resistance. Lipid abnormalities in CD36 deficiency may partly depend on the presence of diabetes, and increased levels of triglyceride and HDL cholesterol may be due to impaired binding of fatty acids and HDL to CD36 and subsequent clearance.
authors.affiliation: Second Department of Internal Medicine, Sapporo Medical University School of Medicine, Japan. furuhasi@sapmed.ac.jp
authors.forename: Masato
authors.initials: M
authors.lastname: Furuhashi
authors.forename: Nobuyuki
authors.initials: N
authors.lastname: Ura
authors.forename: Tomoaki
authors.initials: T
authors.lastname: Nakata
authors.forename: Kazuaki
authors.initials: K
authors.lastname: Shimamoto
mesh_terms: D000368:Aged; D001786:Blood Glucose / Q000032:analysis; D018955:CD36 Antigens / Q000378:metabolism*; D016022:Case-Control Studies; D008076:Cholesterol, HDL / Q000097:blood; D003924:Diabetes Mellitus, Type 2 / Q000150:complications*; D005260:Female; D006442:Glycated Hemoglobin / Q000032:analysis; D006706:Homeostasis; D006801:Humans; D007333:Insulin Resistance; D008055:Lipids / Q000097:blood*; D008297:Male; D008661:Metabolism, Inborn Errors / Q000150:complications / Q000503:physiopathology; D008875:Middle Aged; D008954:Models, Biological; D009994:Osmolar Concentration; D014280:Triglycerides / Q000097:blood
chemical_list: D001786:Blood Glucose; D018955:CD36 Antigens; D008076:Cholesterol, HDL; D006442:Glycated Hemoglobin; D008055:Lipids; D014280:Triglycerides