Excess fat accumulation is a key feature of overweight and obesity that is mainly driven by nutrient overload and insufficient physical activity. White adipose tissue displays lipid overload and hypertrophy accompanied by macrophages infiltration, hypoxia, inflammation and excess production of reactive oxygen species (ROS). An inflammatory response and ROS production are also evident in other metabolism regulating tissues and organs such as skeletal muscle, liver, pancreas and hypothalamus, contributing to a chronic inflammatory state, redox status disturbances and metabolic complications. There is overwhelming evidence showing that adults with overweight/obesity exhibit lower glutathione (GSH) levels in blood erythrocytes, skeletal muscle cells and subcutaneous and visceral adipose tissue cells. GSH, a tripeptide consisting of the amino acids glutamate, cysteine and glycine, is the most abundant thiol-containing antioxidant in the human body and has been, recently, characterized as a novel therapeutic target for the treatment of numerous chronic diseases, due to its potent intracellular redox buffering capacity. Interestingly, lower GSH levels have been associated with diet-induced weight loss resistance, while enhancement of GSH levels through N-acetylcysteine (NAC) supplementation reduces markers of oxidative stress, inflammation, insulin resistance, hypertension, endothelia dysfunction and improves vitamin D metabolism. NAC is a thiol donor that elicits antioxidant effects by (i) directly scavenging ROS and (ii) providing reduced cysteine through deacetylation, which supports the biosynthesis of endogenous GSH via the activity of γ-glutamylcysteine synthase. The aim of this study is to investigate whether NAC supplementation can enhance the exercise training-induced improvements on physical fitness and metabolic health in adult men and women with overweight/obesity.
Age range
30 Years – 45 Years
Sex
ALL
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Change in body weight (kg)
Timeframe: At baseline, 6 weeks and 12 weeks
Change in waist circumference
Timeframe: At baseline, 6 weeks and 12 weeks
Change in hip circumference
Timeframe: At baseline, 6 weeks and 12 weeks
Change in fat mass (kg)
Timeframe: At baseline, 6 weeks and 12 weeks
Change in body fat percent (%)
Timeframe: At baseline, 6 weeks and 12 weeks
Change in fat free mass (kg)
Timeframe: At baseline, 6 weeks and 12 weeks
Change in lean body mass (kg)
Timeframe: At baseline, 6 weeks and 12 weeks
Change in liver fat infiltration
Timeframe: At baseline and 12 weeks
Change in cardiorespiratory fitness
Timeframe: At baseline, 6 weeks and 12 weeks
Change in lower body muscle strength
Timeframe: At baseline, 6 weeks and 12 weeks
Change in upper body muscle strength
Timeframe: At baseline, 6 weeks and 12 weeks
Change in reduced glutathione (GSH) concentration
Timeframe: At baseline, 6 weeks and 12 weeks
Change in oxidized glutathione (GSSG) concentration
Timeframe: At baseline, 6 weeks and 12 weeks
Change in glutathione peroxidase (GPx) activity
Timeframe: At baseline, 6 weeks and 12 weeks
Change in glutathione reductase (GR) activity
Timeframe: At baseline, 6 weeks and 12 weeks
Change in catalase activity
Timeframe: At baseline, 6 weeks and 12 weeks
Change in superoxide dismutase (SOD) activity
Timeframe: At baseline, 6 weeks and 12 weeks
Change in malondialdehyde concentration
Timeframe: At baseline, 6 weeks and 12 weeks
Change in C-reactive protein (CRP) concentration
Timeframe: At baseline, 6 weeks and 12 weeks
Change in TNF-α concentration
Timeframe: At baseline, 6 weeks and 12 weeks
Change in interleukin-6 (IL-6) concentration
Timeframe: At baseline, 6 weeks and 12 weeks
Change in HDL cholesterol concentration
Timeframe: At baseline, 6 weeks and 12 weeks
Change in LDL cholesterol concentration
Timeframe: At baseline, 6 weeks and 12 weeks
Change in total cholesterol concentration
Timeframe: At baseline, 6 weeks and 12 weeks
Change in triglycerides concentration
Timeframe: At baseline, 6 weeks and 12 weeks
Change in serum glutamic-oxaloacetic transaminase (SGOT/AST) concentration
Timeframe: At baseline, 6 weeks and 12 weeks
Alanine Aminotransferase (SGPT/ALT) concentration
Timeframe: At baseline, 6 weeks and 12 weeks
Change in Gamma-glutamyl transpeptidase (γ-GT) concentration
Timeframe: At baseline, 6 weeks and 12 weeks
Change in fetuin-A concentration
Timeframe: At baseline, 6 weeks and 12 weeks
Change in alkaline phosphatase (ALP) concentration
Timeframe: At baseline, 6 weeks and 12 weeks
Change in glucose concentration
Timeframe: At baseline, 6 weeks and 12 weeks
Change in glycated hemoglobin (HbA1c) concentration
Timeframe: At baseline, 6 weeks and 12 weeks
Change in insulin concentration
Timeframe: At baseline, 6 weeks and 12 weeks