scholarly journals Obesity and Male Reproduction: Do Sirtuins Play a Role?

2022 ◽  
Vol 23 (2) ◽  
pp. 973
Author(s):  
Federica Barbagallo ◽  
Sandro La La Vignera ◽  
Rossella Cannarella ◽  
Laura M. Mongioì ◽  
Vincenzo Garofalo ◽  
...  

Obesity is a major current public health problem of global significance. A progressive sperm quality decline, and a decline in male fertility, have been reported in recent decades. Several studies have reported a strict relationship between obesity and male reproductive dysfunction. Among the many mechanisms by which obesity impairs male gonadal function, sirtuins (SIRTs) have an emerging role. SIRTs are highly conserved nicotinamide adenine dinucleotide (NAD+)-dependent deacetylases that play a role in gene regulation, metabolism, aging, and cancer. SIRTs regulate the energy balance, the lipid balance, glucose metabolism, and adipogenesis, but current evidence also indicates a role for SIRTs in male reproduction. However, the majority of the studies have been conducted in animal models and very few have been conducted with humans. This review shows that SIRTs play an important role among the molecular mechanisms by which obesity interferes with male fertility. This highlights the need to deepen this relationship. It will be of particular interest to evaluate whether synthetic and/or natural compounds capable of modifying the activity of SIRTs may also be useful for the treatment of obesity and its effects on gonadal function. Although few studies have explored the role of SIRT activators in obesity-induced male infertility, some molecules, such as resveratrol, appear to be effective in modulating SIRT activity, as well as counteracting the negative effects of obesity on male fertility. The search for strategies to improve male reproductive function in overweight/obese patients is a challenge and understanding the role of SIRTs and their activators may open new interesting scenarios in the coming years.

Antioxidants ◽  
2019 ◽  
Vol 8 (8) ◽  
pp. 268 ◽  
Author(s):  
Izhar Hyder Qazi ◽  
Christiana Angel ◽  
Haoxuan Yang ◽  
Evangelos Zoidis ◽  
Bo Pan ◽  
...  

Selenium (Se) is an important trace mineral having many essential roles at the cellular and organismal levels in animal and human health. The biological effects of Se are mainly carried out by selenoproteins (encoded by 25 genes in humans and 24 in mice). As an essential component of selenoproteins, Se performs structural and enzymic roles; in the latter context it is well known for its catalytic and antioxidative functions. Studies involving different animal models have added great value to our understanding regarding the potential implications of Se and selenoproteins in mammalian fertility and reproduction. In this review, we highlight the implications of selenoproteins in male fertility and reproduction followed by the characteristic biological functions of Se and selenoproteins associated with overall male reproductive function. It is evident from observations of past studies (both animal and human) that Se is essentially required for spermatogenesis and male fertility, presumably because of its vital role in modulation of antioxidant defense mechanisms and other essential biological pathways and redox sensitive transcription factors. However, bearing in mind the evidences from mainstream literature, it is also advisable to perform more studies focusing on the elucidation of additional roles played by the peculiar and canonical selenoproteins i.e., glutathione peroxidase 4 (GPX4) and selenoprotein P (SELENOP) in the male reproductive functions. Nevertheless, search for the elucidation of additional putative mechanisms potentially modulated by other biologically relevant selenoproteins should also be included in the scope of future studies. However, as for the implication of Se in fertility and reproduction in men, though a few clinical trials explore the effects of Se supplementation on male fertility, due to inconsistencies in the recruitment of subjects and heterogeneity of designs, the comparison of such studies is still complicated and less clear. Therefore, further research focused on the roles of Se and selenoproteins is awaited for validating the evidences at hand and outlining any therapeutic schemes intended for improving male fertility. As such, new dimensions could be added to the subject of male fertility and Se supplementation.


2021 ◽  
Vol 6 (6) ◽  
pp. 275-281
Author(s):  
S. S. Ostrovska ◽  
◽  
S. V. Abramov ◽  
I. A. Pisarevska ◽  
O. S. Trushenko ◽  
...  

The purpose of the review of foreign literature was to analyze current research on the effects of cadmium on male reproductive function. Results. According to the researcher data, at least 15–20% of cases of fertility decline in males fall on infertility. The etiology of this phenomenon in 50% of cases remains unknown, however, increasing environmental pollution contributes to a constant increase in male infertility. One of the most toxic pollutants is cadmium. Numerous animal model studies and human epidemiological studies indicate an adverse effect of cadmium on male fertility. Smoking is an important source of cadmium, which is absorbed into the human body. In vitro studies confirm the deleterious effects of cigarette smoke compounds on sperm motility and spermatozoon parameters. Depending on the concentration, nicotine suppresses the progressive motility of the spermatozoon parameters, starting from the lowest concentration used (1 ng/ml). Likewise, it decreases the percentage of viable spermatozoon parameters and increases the amount of spermatozoon parameters in late apoptosis with altered chromatin compactness or DNA fragmentation already after 3 hours of incubation. On average, the daily intake of cadmium in humans is 1.06 μg/kg body weight, the half-life of cadmium is more than 20-40 years, which causes its accumulation in the body. The testicles are the organ in which cadmium is stored in large quantities. Studies have shown that the testicles are extremely sensitive to cadmium because these organs are characterized by intense cellular activity, where vital spermatogenesis processes take place. Exposure to cadmium leads to reproductive tract abnormalities such as cryptorchidism and hypospadias, testicular cancer, subfertility or infertility, called testicular dysgenesis syndrome. In the genesis of the testicles during the embryonic and neonatal periods, Sertoli’s cells play a critical role, the development of which is influenced by cadmium. Exposure to cadmium (1-2 mg/kg, subcutaneously) in pregnant and lactating rats causes vacuolization of Sertoli’s cells and loss of cells in the epithelium of the seminiferous tubules in adult animals. Cadmium inhibits proliferation, induces apoptosis and DNA damage in immature Sertoli’s cells. Perinatal exposure to cadmium affects the development and function of fetal Leydig cells, which are endocrine cells in the testicle. In pregnant rats that received a single dose of cadmium (0.25, 0.5, and 1.0 mg/kg, intraperitoneally), synthesis of testosterone in the fetal tests was significantly reduced, while gene expression in cells was suppressed, and the androgen-dependent formation process was reduced. The mechanism by which cadmium mediates impaired male fertility is also associated with the production of reactive oxygen species in the testicles, which leads to oxidative stress that interferes with the development and functioning of the spermatozoon parameters. Exposure to cadmium, for both environmental and occupational reasons, can contribute to a decrease in the quality of human sperm, which confirms high toxicity of cadmium. Conclusion. Thus, in humans and other mammals, cadmium damages the male reproductive system, disrupts its structure, including the vascular system of the testicles, leads to DNA damage, inhibits functions of germ cells, leads to loss of sperm quality and quantity, sub-fertility or infertility


2020 ◽  
Vol 16 ◽  
Author(s):  
Hamed Heydari ◽  
Rafighe Ghiasi ◽  
Saber Ghaderpour ◽  
Rana Keyhanmanesh

Introduction: Obesity resulted by imbalance between the intake of energy and energy consumption can lead to growth and metabolic disease development in people. Both in obese men and animal models, several studies indicate that obesity leads to male infertility. Objective: This review has discussed some mechanisms involved in obesity-induced male infertility. Method: Online documents were searched through Science Direct, Pubmed, Scopus, and Google Scholar websites dating from 1959 to recognize studies on obesity, kisspeptin, leptin, and infertility. Results: Obesity induced elevated inflammatory cytokines and oxidative stress can affect male reproductive functions including spermatogenesis disorders, reduced male fertility power and hormones involved in hypothalamus-pituitarygonadal axis. Conclusion: There is significant evidence that obesity resulted in male infertility. obesity has negative effect on male reproductive function via several mechanisms such as inflammation and oxidative stress.


2020 ◽  
Vol 20 (2) ◽  
pp. 198-202 ◽  
Author(s):  
Mohammad Motamedifar ◽  
Yalda Malekzadegan ◽  
Parisa Namdari ◽  
Behzad Dehghani ◽  
Bahia Namavar Jahromi ◽  
...  

Introduction: Infertility considered as a social and public health issue and estimated that most of these infertile couples are residents of developing countries. Infectious diseases including the history of Sexually Transmitted Infections (STIs) may impact on male reproductive function. Therefore, the present study aimed to investigate the prevalence of bacterial contaminants of semen and probable association with sperm quality of infertile men in Iranian population. Methods: The study population consisted of 200 infertile men and 150 fertile men attending an infertility Center in southwestern Iran during the study period in 2015. The assessment of sperm parameters was according to the World Health Organization (WHO) guidelines. The presumptive pathogens were identified using standard microbiology tests and confirmed by specific PCR primers. Results: The prevalence of bacteriospermia in the semen of the infertile group was significantly higher than that in the fertile group (48% vs. 26.7%, P <0.001). The microbiological analysis of samples showed that the most abundant species of bacteria in semen of infertile men were Chlamydia trachomatis (12.5%) followed by Neisseria gonorrhoeae (11%). On the other hand, in the control group, Lactobacillus spp. (17.3%) was the most isolated pathogen. Results showed that the presence of N. gonorrhoeae, C. trachomatis, Mycoplasma genitalium, Haemophilus, and Klebsiella was significantly associated with sperm abnormality. Conclusion: Based on our findings, it seems that bacteriospermia is associated with alterations in the properties of semen which may lead to a decrease in the fertilization potential of sperm. Therefore, immediate and appropriate treatment is necessary before investigating every other possible cause of infertility.


2021 ◽  
Vol 12 (6) ◽  
Author(s):  
Xiaochun Chi ◽  
Weiwei Luo ◽  
Jiagui Song ◽  
Bing Li ◽  
Tiantian Su ◽  
...  

AbstractKindlin-2 is known to play important roles in the development of mesoderm-derived tissues including myocardium, smooth muscle, cartilage and blood vessels. However, nothing is known for the role of Kindlin-2 in mesoderm-derived reproductive organs. Here, we report that loss of Kindlin-2 in Sertoli cells caused severe testis hypoplasia, abnormal germ cell development and complete infertility in male mice. Functionally, loss of Kindlin-2 inhibits proliferation, increases apoptosis, impairs phagocytosis in Sertoli cells and destroyed the integration of blood-testis barrier structure in testes. Mechanistically, Kindlin-2 interacts with LATS1 and YAP, the key components of Hippo pathway. Kindlin-2 impedes LATS1 interaction with YAP, and depletion of Kindlin-2 enhances LATS1 interaction with YAP, increases YAP phosphorylation and decreases its nuclear translocation. For clinical relevance, lower Kindlin-2 expression and decreased nucleus localization of YAP was found in SCOS patients. Collectively, we demonstrated that Kindlin-2 in Sertoli cells is essential for sperm development and male reproduction.


2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Elisabetta Catalani ◽  
Clara De Palma ◽  
Cristiana Perrotta ◽  
Davide Cervia

Neuropeptides drive a wide diversity of biological actions and mediate multiple regulatory functions involving all organ systems. They modulate intercellular signalling in the central and peripheral nervous systems as well as the cross talk among nervous and endocrine systems. Indeed, neuropeptides can function as peptide hormones regulating physiological homeostasis (e.g., cognition, blood pressure, feeding behaviour, water balance, glucose metabolism, pain, and response to stress), neuroprotection, and immunomodulation. We aim here to describe the recent advances on the role exerted by neuropeptides in the control of autophagy and its molecular mechanisms since increasing evidence indicates that dysregulation of autophagic process is related to different pathological conditions, including neurodegeneration, metabolic disorders, and cancer.


Development ◽  
2000 ◽  
Vol 127 (1) ◽  
pp. 143-153 ◽  
Author(s):  
D. Thepot ◽  
J.B. Weitzman ◽  
J. Barra ◽  
D. Segretain ◽  
M.G. Stinnakre ◽  
...  

JunD is one of three mammalian Jun proteins that contribute to the AP-1 transcription factor complex. Distinct regulation and functions have been proposed for each Jun member, but less is known about the biological functions of each of these proteins in vivo. To investigate the role of JunD, we have inactivated the murine gene by replacement with a bacterial lacZ reporter gene. Embryonic JunD expression was initially detected in the developing heart and cardiovascular system. Subsequent broadening phases of JunD expression were observed during embryonic development and expression in the adult was widespread in many tissues and cell lineages. Mutant animals lack JunD mRNA and protein and showed no evidence of upregulation of c-Jun and JunB mRNA levels. In contrast to the other two Jun members, homozygous JunD−/− mutant animals were viable and appeared healthy. However, homozygous JunD−/− animals showed a reduced postnatal growth. Furthermore, JunD−/− males exhibited multiple age-dependent defects in reproduction, hormone imbalance and impaired spermatogenesis with abnormalities in head and flagellum sperm structures. No defects in fertility were observed in JunD−/− female animals. These results provide evidence for redundant functions for members of the Jun family during development and specific functions for JunD in male reproductive function.


2020 ◽  
Vol 2020 ◽  
pp. 1-13 ◽  
Author(s):  
Xuejie Yi ◽  
Donghui Tang ◽  
Shicheng Cao ◽  
Tao Li ◽  
Haining Gao ◽  
...  

This study is aimed at investigating the effect of different exercise loads on the reproductive function of obese male mice and the underlying mechanisms. Male mice with high-fat diet-induced obesity were divided into obesity control (OC), obesity moderate-load exercise (OME), and obesity high-load exercise (OHE) groups. The OME and OHE groups were subjected to swimming exercise 5 days per week over a duration of 8 weeks, with the exercise load progressively increased to 2 h per day in the OME group and 2 h twice per day in the OHE group. In the OC group mice without exercise regimen, we observed a decrease in mRNA expression of antioxidant enzymes, increase in free radical products, upregulation of mRNA and protein expression of nuclear factor-κB and proinflammatory cytokines, inhibition of mRNA and protein expression of testosterone synthases, decrease in the serum testosterone level and sperm quality, and increase in sperm apoptosis. Although both moderate-load exercise and high-load exercise reduced body fat, only moderate-load exercise effectively alleviated obesity-induced oxidative stress, downregulated the expression of nuclear factor-κB and proinflammatory cytokines, and reversed the decrease in mRNA and protein expression of testosterone synthases, serum testosterone level, and sperm quality. These changes were not observed in the OHE group mice. Obesity-induced testicular oxidative stress and inflammatory response decreased testosterone synthesis and sperm quality. Moderate-load exercise alleviated the negative effect of obesity on male reproductive function by decreasing testicular oxidative stress and inflammatory responses. Although high-load exercise effectively reduced body fat, its effects on alleviating oxidative stress and improving male reproductive function were limited.


2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Mary K. Samplaski ◽  
Trustin Domes ◽  
Keith A. Jarvi

Introduction. Chlamydia trachomatis is an established cause of tubal factor infertility; however its role in male fertility is not as clear. We sought to determine the prevalence of Chlamydia in infertile men and evaluate its impact on male reproductive potential. Materials and Methods. We compared the incidence of Chlamydia in our infertile male population with that reported in the literature. We then reviewed the impact of Chlamydia infection on male fertility. Results. The incidence of Chlamydia infection in our population of infertile men was 0.3%. There is considerable variability in the reported incidence, likely due to variation in the population studied, and detection technique. The optimal testing method and sample are presently unclear. The effect of Chlamydia on male reproductive function is also variable in the literature, but appears to be relatively minimal and may be related primarily to sperm DNA fragmentation or female partner transmission. Conclusions. The prevalence of Chlamydia in the infertile male population is low and routine testing is not supported by the literature. For high-risk infertile men, nucleic acid testing of urine +/− semen is the most sensitive method to detect Chlamydia. A validated testing system for semen needs to be developed, so that a standardized methodology can be recommended. In this way the full implications of Chlamydia on male fertility can be elucidated.


2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Ning Zhang ◽  
Yong-Ping Wu ◽  
Sheng-Jun Qian ◽  
Chong Teng ◽  
Shuai Chen ◽  
...  

Platelet-rich plasma (PRP) therapy is a recently developed technique that uses a concentrated portion of autologous blood to try to improve and accelerate the healing of various tissues. There is a considerable interest in using these PRP products for the treatment used in bone deficiency healing. Because PRP products are safe and easy to prepare and administer, there has been increased attention toward using PRP in numerous clinical settings. The benefits of PRP therapy appear to be promising, and many investigators are exploring the ways in which this therapy can be used in the clinical setting. At present, the molecular mechanisms of bone defect repair studies have focused on three aspects of the inflammatory cytokines, growth factors and angiogenic factors. The role of PRP works mainly through these three aspects of bone repair. The purpose of this paper is to review the current evidence on the mechanism of the effect of PRP in bone deficiency healing.


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