4.3 Article

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

期刊

FEBS OPEN BIO
卷 13, 期 4, 页码 763-778

出版社

WILEY
DOI: 10.1002/2211-5463.13589

关键词

high-fat diet (HFD); mitochondria; obesity; oxidative stress; sperm

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Obesity is a metabolic disease that can cause male infertility or subfertility through oxidative stress. This study found that obesity impairs sperm mitochondrial integrity and function, leading to reduced sperm quality in overweight/obese men and mice on a high-fat diet. The excessive fat intake caused increased oxidative stress levels and decreased sperm motility by affecting mitochondrial structure and function. Clinical studies also supported these findings, showing a correlation between obesity and lower sperm quality. These results highlight the importance of maintaining a healthy weight for male fertility.
Obesity is a systemic metabolic disease that can induce male infertility or subfertility through oxidative stress. The aim of this study was to determine how obesity impairs sperm mitochondrial structural integrity and function, and reduces sperm quality in both overweight/obese men and mice on a high-fat diet (HFD). Mice fed the HFD demonstrated higher body weight and increased abdominal fat content than those fed the control diet. Such effects accompanied the decline in antioxidant enzymes, such as glutathione peroxidase (GPX) and catalase and superoxide dismutase (SOD) in testicular and epidydimal tissues. Moreover, malondialdehyde (MDA) content significantly increased in sera. Mature sperm in HFD mice demonstrated higher oxidative stress, including increased mitochondrial reactive oxygen species (ROS) levels and decreased protein expression of GPX1, which may impair mitochondrial structural integrity and reduce mitochondrial membrane potential (MMP) and ATP production. Moreover, cyclic AMPK phosphorylation status increased, whereas sperm motility declined in the HFD mice. Clinical studies demonstrated that being overweight/obese reduced SOD enzyme activity in the seminal plasma and increased ROS in sperm, accompanied by lower MMP and low-quality sperm. Furthermore, ATP content in the sperm was negatively correlated with increases in the BMI of all clinical subjects. In conclusion, our results suggest that excessive fat intake had similar disruptive effects on sperm mitochondrial structure and function, as well as oxidative stress levels in humans and mice, which in turn induced lower sperm motility. This agreement strengthens the notion that fat-induced increases in ROS and impaired mitochondrial function contribute to male subfertility.

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