ECE2009 Poster Presentations Diabetes and Cardiovascular (103 abstracts)
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
Andi Masha 1 , Loredana Brocato 1 , Stefano Dinatale 1 , Cinzia Mascia 2 , Fiorella Biasi 2 & Valentino Martina 1
1Division of Endocrinology, Department of Internal Medicine, University of Turin, Turin, Italy; 2Department of Clinical and Biological Sciences, University of Turin, Turin, Italy.
Introduction: Post-prandial hyperglycaemia seems to play a pivotal role in the pathogenesis of cardiovascular complications of diabetes mellitus, as it leads to oxidative stress which in turn causes reduced NO bioavailability that produce endothelial activation.
Aim: Aim of the study was to assure that the administration of N-acetylcysteine (NAC), thiolic antioxidant, is able to decrease oxidation status and endothelial activation after a high-glucose content meal.
Subjects and methods: Ten patients with type 2 diabetes mellitus (DMT2) (Group 1) and 10 normal subjects (Group 2) assumed a high-glucose content meal without (phase A) or after (phase B) the administration of NAC. Glycaemia, insulinemia, ICAM-1, VCAM-1, E-selectin, malonaldehyde (MDA) and 4-hydroxynonenal (HNE) were assessed at 0, +30′,+60′,+90′,+120′ and +180′.
Results: During phase A in group 1, only HNE and MDA levels increased after the meal assumption (+60′: 7.7 (6.2–8.5) vs 6.9 (5.6–8.0), P<0.05 and 4.8 (3.6–5.3) vs 4.3 (3.7–4.9), P<0.02 respectively); all parameters remained unchanged in group 2. During phase B, in group 1, HNE, MDA, VCAM-1 and E-selectin levels after the meal were lower than those in phase A (see Table), while no change for all variables were observed in group 2.
Conclusions: A high-glucose meal produces an increase in oxidation parameters in DMT2. NAC reduces the oxidative stress and, subsequently, reduces the endothelial activation. In conclusion, NAC could be efficacious in the slackening of the progression of vascular damage in DMT2.
| 0′ | +30′ | +60′ | +90′ | +120′ | +180′ | |
| HNE | 6.9 (4.9–7.3) | 7.2 (4.6–7.8)* | 7.3 (5.1–8.1)* | 7.1 (5.1–7.9)* | 6.8 (5.0–7.9)* | 7.0 (4.8–7.9) |
| MDA | 3.9 (3.0–4.4) | 4.2 (2.9–4.7)* | 4.3 (3.0–4.7)* | 4.1 (3.0–4.8)* | 4.2 (2.9–4.6)* | 4.1 (3.0–4.8)* |
| VCAM-1 | 1.1 (0.7–1.8) | 1.2 (0.7–1.8) | 1.2 (0.6–1.9)* | 1.2 (0.7–1.8)* | 1.1 (0.7–1.9) | 1.1 (0.7–1.7)* |
| E-SEL | 3.1 (2.6–4.3) | 3.1 (2.0–3.8)* | 3.1 (2.0–3.6)* | 2.7 (2.0–3.7)* | 2.8 (1.8–3.9)* | 2.7 (2.1–3.9)* |
| *P<0.05 respect to same time in phase A. | ||||||
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