Obesity leads to higher risk of sperm DNA damage in infertile patients

Dupont, Charlotte; Faure, Céline; Sermondade, Nathalie; Boubaya, Marouane; Eustache, Florence; Clément, Patrice; Briot, Pascal; Berthaut, Isabelle; Lévy, Vincent; Cédrin‐Durnerin, Isabelle; Benzacken, Brigitte; Chavatte‐Palmer, Pascale; Lévy, Rachel

doi:10.1038/aja.2013.65

Cited by 173 publications

(121 citation statements)

References 23 publications

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“…Recently, both clinical and experimental reveal the negative consequences of obesity on male reproductive function. According to the clinical investigation, men with overweight or obesity can decrease sperm quality including sperm concentration, sperm motility, acrosome reaction decline, increased sperm DNA damage and lower embryo implantation rates as well, comparing to those of normal BMI men (Jensen et al 2004, Dupont et al 2013, Samavat et al 2014, Shukla et al 2014, McPherson et al 2015, Soubry et al 2016. In consequence, obesity was associated with a more than 20% increased cases of subfertility and infertility (Cui et al 2016).…”

Section: Introductionmentioning

confidence: 99%

Obesity, a serious etiologic factor for male subfertility in modern society

Liu¹,

Ding²

2017

Reproduction

181

141

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Obesity, defined as excessive accumulation of fat in adipose tissue, is a metabolic disorder resulting from behavioral, environmental and heritable causes. Obesity increases the risks of hypertension, diabetes, cardiovascular disease, sleep apnea, respiratory problems, osteoarthritis and cancer. Meanwhile, the negative impact of obesity on male reproduction is gradually recognized. According to the clinical investigations and animal experiments, obesity is correlated with reductions in sperm concentration and motility, increase in sperm DNA damage and changes in reproductive hormones. Several mechanisms can elucidate the effects of obesity on sperm functions and male subfertility, i.e., the excessive conversion of androgens into estrogens in redundant adipose tissue causes sexual hormone imbalance, subsequently resulting in hypogonadism. Secondly, adipokines produced by adipose tissue induce severe inflammation and oxidative stress in male reproductive tract, directly impairing testicular and epididymal tissues. Moreover, increased scrotal adiposity leads to increase gonadal heat, continuously hurting spermatogenesis. Therefore, obesity alters the systematic and regional environment crucial for spermatogenesis in testis and sperm maturation in epididymis, and finally results in poor sperm quality including decreased sperm motility, abnormal sperm morphology and acrosome reaction, changed membrane lipids and increased DNA damage. Furthermore, recent studies indicate that epigenetic changes may be a consequence of increased adiposity. A major effort to identify epigenetic determinants of obesity revealed that sperm DNA methylation and non-coding RNA modification are associated with BMI changes and proposed to inherit metabolic comorbidities across generations. This review will explain how obesity-related changes in males to influence sperm function and male fertility as well.Reproduction (2017) 154 R123-R131

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Section: Introductionmentioning

confidence: 99%

Obesity, a serious etiologic factor for male subfertility in modern society

Liu¹,

Ding²

2017

Reproduction

181

141

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“…Although controversial, numerous studies show that the quality and quantity of male spermatozoa decline from 1 year to the next [2], with many factors including environmental effects, metabolic dysfunction, and genetic polymorphisms apparently associated with a decline in male reproductive ability [3]; however, only obesity has been shown conclusively to be involved in this phenomenon [4][5][6].…”

Section: Introductionmentioning

confidence: 99%

Protective effects of metformin on reproductive function in obese male rats induced by high-fat diet

Yan

et al. 2015

J Assist Reprod Genet

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Purpose The study aims to elucidate the changes in testicular spermatogenic function in high-fat diet (HFD)-induced obese rats and to evaluate the protective effects of metformin intervention. Methods Male Sprague-Dawley rats (n=18) were randomly divided into a control group (standard diet), an HFD group, and a metformin group (HFD + metformin at 100 mg/kg, once daily by oral gavage). After 8 weeks, rats were euthanized, and the weights of body and testes were measured. Testis and epididymis were dissected and hematoxylin-eosin-stained for histopathological examination and semen parameter analysis. Blood samples were collected for assessment of sex hormones and metabolic parameters (serum glucose, insulin, and leptin). Spermatogenic cell apoptosis was accessed by TUNEL. Results Compared with the control group, the final body weight and weight gain were significantly higher in HFD rats, while the testicle weight and coefficients were lower. In HFD rats, metformin treatment induced weight loss and increased testicle weight (P<0.05). In HFD rats, obvious pathological changes in the testicular tissue were characterized by small, atrophic, and distorted seminiferous tubules and destroyed basement membrane. Metformin treatment protected against the HFD-induced decrease in the number of spermatogonia, Sertoli cells, and Leydig cells (P<0.05); ameliorated the HFD-induced increases in serum glucose, insulin, leptin, and estrogen; and decreased serum testosterone (P<0.05) and reduced the rate of testicular cell apoptosis in obese male rats. Finally, metformin significantly improved semen parameters (including concentration, viability, motility, and normal morphology) in HFD rats (P<0.05). Conclusions HFD-induced obesity in rats results in detrimental effects on spermatogenesis, semen quality, endogenous hormones, and testicular cell apoptosis. Metformin intervention improved the semen parameters, possibly due to its effects on weight loss, increased testicular weight, reduced testicular cell apoptosis, and resulted in restoration of hormonal homeostasis and correction of metabolic disorder.

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“…Recent studies have suggested little relationship between the functional competence of spermatozoa, in terms of their ability to bind to the zona pellucida, and BMI (Sermondade et al 2013a), although a recent metaanalysis has revealed odds ratios for oligozoospermia/ azoospermia of 1.28 (1.06-1.55) for obese and 2.04 (1.59-2.62) for morbidly obese men (Sermondade et al 2013b). A more consistent feature of obese males is the appearance of DNA fragmentation in the spermatozoa in association with oxidative stress (Palmer et al 2012a, 2012b, Dupont et al 2013. The DNA damage associated with obesity may be initiated at the spermatid stage of development while spermatids are differentiating into spermatozoa in a process known as spermiogenesis.…”

Section: Obesitymentioning

confidence: 99%

Age, the environment and our reproductive future: bonking baby boomers and the future of sex

Aitken

2014

Reproduction

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There has never been a greater need for scientists trained in reproductive science. Most developed countries are witnessing unprecedented rates of recourse to assisted conception sitting cheek-by-jowl with high rates of induced abortion. This article addresses these two incongruous faces of reproductive healthcare. Every year at least 44 million abortions are performed worldwide, many under unsafe and insanitary conditions that carry a significant risk to the lives of women deprived of safe, effective methods for controlling their fertility. Although birth control is a complex issue involving myriad social and political factors, the technical vacuum in this area is significant. Through no fault of the family planning authorities, there have been no radically new methods of fertility control since the oral contraceptive pill was introduced in 1960 and even this contribution to planned parenthood has its roots in the biochemistry of the 1920s and 1930s. Moreover, the pharmaceutical industry has, by and large, turned its back on fundamental research activities in this area. At present, our major investment in reproductive healthcare involves treating ever-increasing numbers of couples with assisted reproductive technologies (ART). However, these treatments are often delivered without critically considering the underlying causes of this condition or seriously contemplating the long-term consequences of the current enthusiasm for such therapy. Significantly, the clinical factors underpinning the commitment of couples to ART include advanced maternal age and a variety of lifestyle factors, such as smoking and obesity, which are known to compromise the developmental potential of the oocyte and DNA integrity in spermatozoa.

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Obesity leads to higher risk of sperm DNA damage in infertile patients

Cited by 173 publications

References 23 publications

Obesity, a serious etiologic factor for male subfertility in modern society

Obesity, a serious etiologic factor for male subfertility in modern society

Protective effects of metformin on reproductive function in obese male rats induced by high-fat diet

Age, the environment and our reproductive future: bonking baby boomers and the future of sex

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