title: Fas/Fas-Ligand pathway is impaired in patients with type 2 diabetes. Influence of hypertension and insulin resistance.
abstract: OBJECTIVE
  In type 2 diabetic patients with no cardiac history or symptoms, 1) to evaluate whether the soluble forms of Fas (sFas) and Fas-ligand (sFasL), involved in apoptosis, may be markers of silent coronary disease or related to hypertension or microangiopathic complications; 2) to examine the effect of short-term glycemic control on sFas and sFasL.
  
  
  METHODS
  (1) sFas and sFasL were measured with the ELISA method in 44 asymptomatic diabetic patients, 33 with hypertension, and with a normal myocardial scintigraphy (n=14), with silent myocardial ischemia (SMI) and without (n=15) or with (n=15) significant coronary stenoses; and in 14 controls; (2) sFas and sFasL were measured in 15 poorly controlled diabetic patients before and after 7 days of CSII treatment.
  
  
  RESULTS
  (1) sFas and sFasL differed in the four groups of patients (p=0.003 each). sFas was significantly higher in the patients with SMI without (p=0.035) and with coronary stenoses (p=0.002) than in the control group. sFasL was lower in the three groups of diabetic patients (p<0.05 each) than in control group. In the diabetic population, sFas correlated positively with hypertension (p=0.021), and sFasL negatively with hypertension (p=0.027) and HOMA index in the non-insulin treated patients (p=0.049); (2) sFas did not differ before or after CSII, and there was a marginal decrease in sFasL.
  
  
  CONCLUSIONS
  Fas-mediated apoptosis is involved in type 2 diabetes and might be associated with hypertension and/or its vascular consequences. sFasL might be affected by insulin resistance. sFas and sFasL are not effective markers of SMI.
authors.affiliation: Department of Diabetology-Endocrinology-Nutrition, AP-HP, Paris-Nord University, Jean Verdier Hospital, and Laboratory of Nutrition and Metabolic Diseases, Paris-Nord University, Bondy, France.
authors.forename: E
authors.initials: E
authors.lastname: Cosson
authors.forename: A F
authors.initials: AF
authors.lastname: Bringuier
authors.forename: J
authors.initials: J
authors.lastname: Paries
authors.forename: R
authors.initials: R
authors.lastname: Guillot
authors.forename: J
authors.initials: J
authors.lastname: Vaysse
authors.forename: J R
authors.initials: JR
authors.lastname: Attali
authors.forename: G
authors.initials: G
authors.lastname: Feldmann
authors.forename: P
authors.initials: P
authors.lastname: Valensi
mesh_terms: D000328:Adult; D001786:Blood Glucose / Q000378:metabolism; D001794:Blood Pressure; D015992:Body Mass Index; D003327:Coronary Disease / Q000097:blood / Q000276:immunology; D048909:Diabetes Complications / Q000097:blood / Q000276:immunology*; D003924:Diabetes Mellitus, Type 2 / Q000276:immunology*; D053222:Fas Ligand Protein; D005260:Female; D006801:Humans; D006973:Hypertension / Q000276:immunology*; D007333:Insulin Resistance / Q000276:immunology*; D008055:Lipids / Q000097:blood; D008297:Male; D008562:Membrane Glycoproteins / Q000097:blood / Q000502:physiology*; D011674:Pulse; D019014:fas Receptor / Q000097:blood / Q000502:physiology*
chemical_list: D001786:Blood Glucose; C505661:FASLG protein, human; D053222:Fas Ligand Protein; D008055:Lipids; D008562:Membrane Glycoproteins; D019014:fas Receptor