The complex relationship between obesity and male reproductive function

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In a review article published in the journal Molecular Aspects of Medicine, authors have analyzed current evidence on the impact of obesity on the male reproduction system.

They have thoroughly discussed molecular mechanisms responsible for male infertility in obese or overweight individuals.

Study: Obesity and male fertility disorders. Image Credit: Shidlovski/Shutterstock.comStudy: Obesity and male fertility disorders. Image Credit: Shidlovski/Shutterstock.com

Background

Obesity is considered to be one of the major causes of male infertility globally. An increased body weight is known to impair testicular development and function starting from prenatal age. Moreover, recent evidence shows that obesity can significantly reduce sperm parameters in adults.

According to the World Health Organization, more than one billion people are living with obesity worldwide.

With an ever-increasing prevalence of obesity in the global population, it has become necessary to precisely understand the relationship between obesity and male reproductive dysfunctions.

Impact of obesity on male infertility

A body mass index (BMI) of 30kg/m2 or more is defined as obesity. The body fat percentages of more than 25% in men and 30% in women are also described as obesity, which are often poorly correlated with BMI in the context of obesity diagnosis.

Studies conducted on couples with an obese male partner have shown that male obesity can significantly increase the risk of infertility. However, studies investigating the direct effect of obesity on conventional sperm parameters have produced mixed or conflicting results.

Studies involving couples undergoing fertility-related treatments have shown that obesity does not have any significant impact of obesity on sperm count, morphology, and motility.

In contrast, findings of meta-analyses have indicated that obesity can reduce total sperm count, sperm concentration, semen volume, sperm vitality, and total sperm motility.

One most recent meta-analysis, including studies following the 2010 WHO manual for sperm parameter analysis, has shown that obesity can significantly reduce total sperm count, sperm concentration, and sperm progressive, and total motility.

This study has also shown that obesity affects overall sperm quality through the induction of hypogonadism (reduced production of male sex hormones).

Regarding sperm bio-functional parameters, evidence indicates that obesity can lead to sperm DNA fragmentation and reduced mitochondrial membrane potential. These parameters might be associated with reduced sperm quality and motility.

Regarding serum hormone levels, evidence indicates that obesity can reduce testosterone and sex hormone-binding globulin levels and increase estrogen levels.

Mechanisms involved in obesity-related male infertility

One of the potential factors responsible for hypogonadism is excess visceral fat deposition. Hypogonadism is associated with excessive conversion of testosterone into 17ß-estradiol by adipocytes, which further promotes the secretion of sex hormone-binding globulin by the liver.

This protein can bind to testosterone and inhibit its biological functions. Furthermore, low blood levels of testosterone due to hypogonadism can trigger fat accumulation in the body.

A reduced testosterone can lead to impaired proliferation and differentiation of Sertoli cell (somatic cells of the testis) and spermatogonial stem cells, negatively affecting spermatogenesis or sperm cell production.

A high blood estrogen level due to hypogonadism can also negatively affect male reproductive system by inhibiting the release of lactate (an essential substrate) to germ cells, as well as by impairing the integrity of blood-testis barrier.

Increased visceral fat can induce insulin resistance, reducing sex hormone-binding globulin secretion and subsequent induction in free estrogen levels. Free estrogen and inflammatory mediators produced due to insulin resistance can negatively affect the hypothalamic-pituitary-gonadal axis.

Insulin resistance can also interfere with follicle-stimulating hormone signaling pathways at the testicular level, leading to impaired spermatogenesis.

An increased insulin level in the blood can impair the growth, proliferation, metabolism, and survival of testicular cells, which in turn can impair male reproductive functions.

Obesity-related low-grade chronic inflammation can influence male reductive functions in many ways. Increased production of pro-inflammatory cytokines can regulate Leydig cell function and subsequently reduce testosterone production.

Obesity-related chronic inflammation can also increase the production of free radicals, leading to sperm DNA damage and reduced sperm quality.

Obesity can affect the levels of adipokines produced by fat cells. These adipokines, including adiponectin, chemerin, leptin, resistin, and visfatin, play vital roles in modulating the immune, metabolism, and reproductive systems.

Leptin is the most studied adipokine that regulates food intake, reproductive functions, and proinflammatory immune responses. A high-fat diet is known to induce leptin resistance in obese people. Highly increased blood levels of leptin characterize this condition.

An increased leptin level can reduce lactate dehydrogenase activity and activate the PI3K/AKT/mTOR signaling pathway, leading to reduced lactate production by Sertoli cells and impaired nutritional support to germ cells.

Sirtuins are NAD+-dependent deacetylases that play a role in modulating spermatogenesis. Sirtuin 1-knock-out mice have been found to have reduced sperm count and increased sperm DNA fragmentation.

Gut hormones, such as ghrelin, Glucagon-like peptide-1, and glucose-dependent insulinotropic polypeptide, secreted by gastrointestinal tract cells, play important roles in regulating lipid and glucose metabolism. An increased secretion of these hormones can lead to impaired functioning of Sertoli cells and Leydig cells.

The gut microbiota provides essential nutrients and factors required for testicular function. Any alteration in gut microbiota composition and function can lead to local inflammation, which in turn can cause Leydig cell death, disrupted blood-testicular-barrier, and abnormal spermatogenesis.

Sperm RNAs, including messenger RNAs (mRNAs), long non-coding RNAs (lncRNAs), micro RNAs (miRNAs), Piwi-interacting RNAs (piRNAs), and transfer of RNA-derived small RNAs (tsRNAs), play vital roles in spermatogenesis, fertilization, and embryo development.

Certain sperm miRNAs have been found to induce inflammatory responses and impair iron homeostasis, glucose metabolism, meiotic recombination, fertilization, and sperm maturation and motility.

Journal reference:
Dr. Sanchari Sinha Dutta

Written by

Dr. Sanchari Sinha Dutta

Dr. Sanchari Sinha Dutta is a science communicator who believes in spreading the power of science in every corner of the world. She has a Bachelor of Science (B.Sc.) degree and a Master's of Science (M.Sc.) in biology and human physiology. Following her Master's degree, Sanchari went on to study a Ph.D. in human physiology. She has authored more than 10 original research articles, all of which have been published in world renowned international journals.

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