Abstract

In recent decades, the worldwide prevalence of obesity has risen dramatically and is currently estimated to be around 20%. Obesity is linked to an increased risk of comorbidities and premature mortality. Several studies have shown that obesity negatively impacts male fertility through various mechanisms. This review aims to investigate the molecular mechanisms through which obesity impairs male reproduction, including obesity-associated hypogonadism and its effects on spermatogenesis, chronic inflammation, and oxidative stress. Obesity negatively impacts both conventional and biofunctional sperm parameters, and it also induces epigenetic changes that can be transferred to offspring. Moreover, obesity-related diseases are linked to a dysregulation of adipocyte function and micro-environmental inflammatory processes. The dysregulated adipokines significantly influence insulin signaling, and they may also have a detrimental effect on testicular function. Sirtuins can also play an important role in inflammatory and metabolic responses in obese patients. Understanding the molecular mechanisms that are involved in obesity-induced male infertility could increase our ability to identify novel targets for the prevention and treatment of obesity and its related consequences.

Highlights

  • Obesity is defined as an abnormal or excessive accumulation of fat

  • Non-esterified fatty acids (NEFA) that are produced by hypertrophic adipocytes induce local macrophages to secrete high levels of tumor-necrosis factor α (TNFα), which, in turn, stimulates adipocytes to produce more non-esterified fatty acids (NEFA), pro-inflammatory cytokines (interleukin 1ß (IL1β) and IL6), acute phase proteins, and chemokines [+(C-C motif chemokine ligand-2 (CCL2) or monocyte attractant protein-1 (MCP-1)), which attract more monocytes/macrophages within adipose tissue [51]

  • An unhealthy attitude towards food and a sedentary lifestyle has greatly increased the prevalence of obesity in Western countries

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Summary

Introduction

Obesity is defined as an abnormal or excessive accumulation of fat. According to the World Health Organization (WHO), a body mass index (BMI) that is greater than or equal to 25 kg/m2 is classified as overweight, a BMI greater than 30 kg/m2 is considered obesity, and a BMI greater than 40 kg/m2 is considered severe obesity [1]. Obesity is linked to an elevated premature mortality risk [3] and an increased risk of comorbidities These include cerebral–cardiovascular diseases, type 2 diabetes mellitus, hypertension, asthma, sleep apnea syndrome, psychiatric diseases, polycystic ovary syndrome (PCOS), nonalcoholic fatty liver disease (NAFLD), gastrointestinal reflux disease, gallbladder disease, osteoarthritis, and many other endocrine system disorders. All of these can negatively impact a person’s life expectancy and quality of life and may influence one’s reproductive and sexual health [4]. Obesity is a risk factor for some neoplasias and has been associated with a poorer response to cancer therapy. This review aims to investigate the relationship between obesity and male infertility, focusing on the molecular mechanisms through which it negatively affects spermatogenesis, sperm quality, and male reproduction

Epidemiology of Male Fertility in Obesity
Hormonal Changes in Obesity
Obesity and Conventional Sperm Parameters
Leptin
Resistin
Visfatin
Chemerin
10. Obesity and Epigenetic Modifications
Findings
11. Conclusions
Full Text
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