Ex vivo Anti-Senescence Activity of N-Acetylcysteine in Visceral Adipose Tissue of Obese Volunteers.

INTRODUCTION: Excessive visceral adiposity is known to drive the onset of metabolic derangements, mostly involving oxidative stress, prolonged inflammation, and cellular senescence. N-acetylcysteine (NAC) is a synthetic form of l-cysteine with potential antioxidant, anti-inflammatory, and anti-senescence properties. This ex-vivo study aimed to determine the effect of NAC on some markers of senescence including ß-galactosidase activity and p16, p53, p21, IL-6, and TNF-α gene expressions in visceral adipose tissue in obese adults. METHODS: This ex-vivo experimental study involved 10 obese participants who were candidates for bariatric surgery. Duplicate biopsies from the abdominal visceral adipose tissue were obtained from the omentum. The biopsies were treated with or without NAC (5 and 10 mm). To evaluate adipose tissue senescence, beta-galactosidase (ß-gal) activity and the expression of P16, P21, P53, IL-6, and TNF-α were determined. ANOVA test was employed to analyze the varying markers of cellular senescence and inflammation between treatment groups. RESULTS: The NAC at concentrations of 5 mm and 10 mm resulted in a noteworthy reduction ß-gal activity compared to the control group (p < 0.001). Additionally, the expression of P16, P21, and IL-6 was significantly reduced following treatment with NAC (5 mm) and NAC (10 mm) compared to the control group (All p < 0.001). DISCUSSION/CONCLUSION: Taken together, these data suggest the senotherapeutic effect of NAC, as it effectively reduces the activity of SA-ß-gal and the expression of IL-6, P16, and P21 genes in the visceral adipose tissue of obese individuals.

The Impact of Low Advanced Glycation End Products Diet on Metabolic Risk Factors: A Systematic Review and Meta-Analysis of Randomized Controlled Trials.

Several randomized clinical trials have investigated the effect of dietary advanced glycation end products (AGEs) on metabolic syndrome risk factors in adults. However, the results of these studies were conflicting. Therefore, our aim was to assess the effect of dietary AGEs on metabolic syndrome risk factors. We searched the PubMed-MEDLINE, Scopus, Cochrane Databases, Google Scholar, Web of Science, and Embase databases for papers published up to October 2019 that investigated the effect of dietary AGEs on metabolic syndrome risk factors. From the eligible trials, 13 articles were selected for inclusion in this systematic review and meta-analysis. The meta-analysis was performed using a random-effects model. Heterogeneity was determined by I2 statistics and Cochrane Q test. Pooled results from the random-effects model showed a significant reduction for insulin resistance [weighted mean difference (WMD): -1.204; 95% CI: -2.057, -0.358; P = 0.006], fasting insulin (WMD: -5.472 µU/mL; 95% CI: -9.718, -1.234 µU/mL; P = 0.011), total cholesterol (WMD: -5.486 mg/dL; 95% CI: -10.222, -0.747 mg/dL; P = 0.023), and LDL (WMD: -6.263 mg/dL; 95% CI: -11.659, -0.866 mg/dL; P = 0.023) in the low-AGEs groups compared with the high-AGEs groups. There were no changes in the other components of the metabolic syndrome. The results of this review suggest that a diet with a low AGEs content has beneficial effects on insulin resistance, fasting insulin, total cholesterol, and LDL. Moreover, following a diet low in AGEs may be a helpful strategy to decrease the burden of metabolic syndrome risk factors in adults and particularly in patients with diabetes.