title: N-acetylcysteine is able to reduce the oxidation status and the endothelial activation after a high-glucose content meal in patients with Type 2 diabetes mellitus.
abstract: Post-prandial hyperglycemia seems to play a pivotal role in the pathogenesis of the cardiovascular complications of diabetes mellitus, as it leads to an oxidative stress which in turn causes a reduced NO bioavailability. These conditions produce an endothelial activation.
  
  
  OBJECTIVE
  The aim of this study was to assure that the administration of N-acetylcysteine (NAC), thiolic antioxidant, is able to decrease the oxidation status and endothelial activation after a high-glucose content meal.
  
  
  METHODS
  Ten patients with Type 2 diabetes mellitus (DMT2) (Group 1) and 10 normal subjects (Group 2) were studied. They assumed a high-glucose content meal without (phase A) or after (phase B) the administration of NAC. Glycemia, insulinemia, intercellular adhesion molecule 1, vascular adhesion molecule 1 (VCAM-1), E-selectin, malonaldehyde (MDA), and 4-hydroxynonenal (HNE) were assessed at -30, 0, +30, +60, +90, +120, and +180 min with respect to the meal consumption.
  
  
  RESULTS
  During the phase A in Group 1, only HNE and MDA levels increased after the meal assumption; all parameters remained unchanged in Group 2. During the phase B, in Group 1, HNE, MDA, VCAM-1, and E-selectin levels after the meal were lower than those in phase A, while no change for all variables were observed in Group 2.
  
  
  CONCLUSIONS
  A high-glucose meal produces an increase in oxidation parameters in patients with DMT2. The administration of NAC reduces the oxidative stress and, by doing so, reduces the endothelial activation. In conclusion, NAC could be efficacious in the slackening of the progression of vascular damage in DMT2.
authors.affiliation: Department of Internal Medicine, Division of Endocrinology, University of Turin, Corso A.M. Dogliotti 14, 10126 Turin, Italy.
authors.forename: A
authors.initials: A
authors.lastname: Masha
authors.forename: L
authors.initials: L
authors.lastname: Brocato
authors.forename: S
authors.initials: S
authors.lastname: Dinatale
authors.forename: C
authors.initials: C
authors.lastname: Mascia
authors.forename: F
authors.initials: F
authors.lastname: Biasi
authors.forename: V
authors.initials: V
authors.lastname: Martina
mesh_terms: D000111:Acetylcysteine / Q000627:therapeutic use*; D000368:Aged; D000447:Aldehydes / Q000378:metabolism; D016022:Case-Control Studies; D003924:Diabetes Mellitus, Type 2 / Q000188:drug therapy* / Q000378:metabolism; D019040:E-Selectin / Q000378:metabolism; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000378:metabolism; D005260:Female; D016166:Free Radical Scavengers / Q000627:therapeutic use*; D005947:Glucose / Q000008:administration & dosage* / Q000378:metabolism; D038321:Glycemic Index; D006801:Humans; D007328:Insulin / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D008875:Middle Aged; D010084:Oxidation-Reduction; D018384:Oxidative Stress / Q000187:drug effects*; D019518:Postprandial Period; D019010:Vascular Cell Adhesion Molecule-1 / Q000378:metabolism
chemical_list: D000447:Aldehydes; D019040:E-Selectin; D016166:Free Radical Scavengers; D007328:Insulin; D019010:Vascular Cell Adhesion Molecule-1; D008315:Malondialdehyde; D005947:Glucose; C027576:4-hydroxy-2-nonenal; D000111:Acetylcysteine