Obesity-induced oxidative stress and mitochondrial dysfunction negatively affect sperm quality

Area of Science:

• Reproductive biology
• Metabolic disease research
• Oxidative stress mechanisms

Background:

• Obesity is a systemic metabolic disease linked to male infertility via oxidative stress.
• Understanding how obesity affects sperm mitochondrial function is crucial for male reproductive health.

Purpose of the Study:

• To investigate the impact of obesity on sperm mitochondrial integrity and function.
• To assess the reduction in sperm quality in overweight/obese men and mice on a high-fat diet (HFD).

Main Methods:

• Comparative study of mice on HFD versus control diets.
• Analysis of antioxidant enzyme levels (GPX, catalase, SOD) and malondialdehyde (MDA) in tissues and sera.
• Evaluation of sperm oxidative stress markers (ROS, GPX1), mitochondrial membrane potential (MMP), ATP production, and motility.
• Clinical correlation of body mass index (BMI) with sperm quality parameters in human subjects.

Main Results:

• HFD mice showed increased body weight, abdominal fat, and serum MDA, with decreased antioxidant enzymes.
• HFD mice sperm exhibited elevated ROS, reduced GPX1, impaired MMP, lower ATP production, and decreased motility.
• Overweight/obese men displayed reduced seminal plasma SOD, increased sperm ROS, lower MMP, and poorer sperm quality.
• Sperm ATP content negatively correlated with BMI in human subjects.

Conclusions:

• Excessive fat intake disrupts sperm mitochondrial structure and function, increasing oxidative stress in both humans and mice.
• Impaired mitochondrial function and increased reactive oxygen species (ROS) contribute to obesity-induced male subfertility.
• Findings highlight the detrimental effects of obesity on male reproductive health through oxidative stress pathways.