The antioxidant N-Acetylcysteine does not improve glucose tolerance or β-cell function in type 2 diabetes.

Autor: Szkudlinska MA; Division of Metabolism, Endocrinology and Nutrition, VA Puget Sound Health Care System and University of Washington, Seattle, WA. Electronic address: magda3@u.washington.edu., von Frankenberg AD; Post-Graduate Endocrinology Program, School of Medicine, Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil. Electronic address: anize.frankenberg@gmail.com., Utzschneider KM; Division of Metabolism, Endocrinology and Nutrition, VA Puget Sound Health Care System and University of Washington, Seattle, WA. Electronic address: kutzschn@u.washington.edu.
Jazyk: angličtina
Zdroj: Journal of diabetes and its complications [J Diabetes Complications] 2016 May-Jun; Vol. 30 (4), pp. 618-22. Date of Electronic Publication: 2016 Feb 05.
DOI: 10.1016/j.jdiacomp.2016.02.003
Abstrakt: Unlabelled: Hyperglycemia induces oxidative stress and thereby may exacerbate β-cell dysfunction in type 2 diabetes (T2DM). Notably, glutathione (GSH), synthesized from N-Acetylcysteine (NAC), neutralizes reactive oxygen species within cells and is low in individuals with diabetes.
Aim: Determine if NAC supplementation improves β-cell function and glucose tolerance by decreasing oxidative stress in T2DM.
Methods: Thirteen subjects (6M/7F) with T2DM (duration: 0-13 years, median: 2 years), treated with diet/exercise alone (n=7) or metformin (n=6), underwent a 2-h oral glucose tolerance test (OGTT) at baseline, after 2 weeks supplementation with 600 mg NAC orally twice daily, and again after 2 weeks supplementation with 1200 mg NAC twice daily. The following measurements were made: fasting glucose and fructosamine for glycemic control, incremental AUC glucose (0-120 min) for glucose tolerance, and Δ insulin/Δ glucose (0-30 min) for the early insulin response to glucose. Fasting erythrocyte GSH and GSSG (oxidized glutathione) levels, plasma thiobarbituric acid reactive substances (TBARS), and urine F2α isoprostanes were measured to assess oxidative status.
Results: Subjects were middle aged (mean ± SEM: 53.9 ± 3.2 years), obese (BMI 37.3 ± 2.8 kg/m(2)), and relatively well-controlled (HbA1c 6.7 ± 0.3%, 50 mmol/mol). Glycemic control, glucose tolerance, insulin release, and oxidative markers did not change with either dose of NAC.
Conclusions: Based on the lack of any short-term benefit from NAC supplementation on markers of glucose metabolism, β-cell response, and oxidative status, it is unlikely to be a valuable therapeutic approach for treatment of type 2 diabetes.
(Published by Elsevier Inc.)
Databáze: MEDLINE
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