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How much does obesity affect the male reproductive function?

ABSTRACT: Obesity is considered a worldwide epidemic disease. Many pathological conditions have been associated to obesity but the evidence relating to impaired fertility in males with obesity are contrasting. The aim of this review was to evaluate the interplay between obesity and male fertility, analyzing evidence from in vitro and in vivo studies to clinical trials. Obesity seems to be responsible of secondary hypogonadism. Here, we propose a new classification including central, peripheral and testicular factors that may affect the hypothalamic-pituitary-gonadal axis. Moreover, some studies demonstrated a direct action of obesity on sperm count and sperm characteristics, mediated by impaired Sertoli cells function, increased scrotal temperature, oxidative stress and accumulation of toxic substances and liposoluble endocrine disruptors in fat tissue. Recent studies have explored obesity-related epigenetic effects in sperm cells which may cause diseases in offspring. Moreover, not only in females but also males, obesity has been linked to reduced outcomes of in vitro fertilization, with a reduction of pregnancy rate and an increase of pregnancy loss. Finally, we reviewed the effects of weight modifications through diet or bariatric surgery on obesity-related reproductive dysfunction. In this regard, several studies have demonstrated that weight loss has been associated with a restoration of gonadal hormones levels.

SUBMITTER: Bellastella G

PROVIDER: S-EPMC6683183 | biostudies-literature | 2019 Apr

REPOSITORIES: biostudies-literature

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How much does obesity affect the male reproductive function?

Bellastella Giuseppe G Menafra Davide D Puliani Giulia G Colao Annamaria A Savastano Silvia S

International journal of obesity supplements 20190412 1

Obesity is considered a worldwide epidemic disease. Many pathological conditions have been associated to obesity but the evidence relating to impaired fertility in males with obesity are contrasting. The aim of this review was to evaluate the interplay between obesity and male fertility, analyzing evidence from in vitro and in vivo studies to clinical trials. Obesity seems to be responsible of secondary hypogonadism. Here, we propose a new classification including central, peripheral and testicu ...[more]

PMID: 31391924

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Project description:Environmental toxicants, such as cadmium and bisphenol A (BPA) are endocrine disruptors. In utero, perinatal or neonatal exposure of BPA to rats affect the male reproductive function, such as the blood-testis barrier (BTB) integrity. This effect of BPA on BTB integrity in immature rats is likely mediated via a loss of gap junction function at the BTB, failing to coordinate tight junction and anchoring junction function at the site to maintain the immunological barrier integrity. This in turn activates the extracellular signal-regulated kinases 1/2 (Erk1/2) downstream and an increase in protein endocytosis, destabilizing the BTB. The cadmium-induced disruption of testicular dysfunction is mediated initially via its effects on the occludin/ZO-1/focal adhesion kinase (FAK) complex at the BTB, causing redistribution of proteins at the Sertoli-Sertoli cell interface, leading to the BTB disruption. The damaging effects of these toxicants to testicular function are mediated by mitogen-activated protein kinases (MAPK) downstream, which in turn perturbs the actin bundling and accelerates the actin-branching activity, causing disruption of the Sertoli cell tight junction (TJ)-barrier function at the BTB and perturbing spermatid adhesion at the apical ectoplasmic specialization (apical ES, a testis-specific anchoring junction type) that leads to premature release of germ cells from the testis. However, the use of specific inhibitors against MAPK was shown to block or delay the cadmium-induced testicular injury, such as BTB disruption and germ cell loss. These findings suggest that there may be a common downstream p38 and/or Erk1/2 MAPK-based signaling pathway involving polarity proteins and actin regulators that is shared between different toxicants that induce male reproductive dysfunction. As such, the use of inhibitors and/or antagonists against specific MAPKs can possibly be used to "manage" the illnesses caused by these toxicants and/or "protect" industrial workers being exposed to high levels of these toxicants in their work environment.

Project description:BACKGROUND:Tsetse flies (Diptera, Glossinidae) display unique reproductive biology traits. Females reproduce through adenotrophic viviparity, nourishing the growing larva into their modified uterus until parturition. Males transfer their sperm and seminal fluid, produced by both testes and male accessory glands, in a spermatophore capsule transiently formed within the female reproductive tract upon mating. Both sexes are obligate blood feeders and have evolved tight relationships with endosymbionts, already shown to provide essential nutrients lacking in their diet. However, the partnership between tsetse and its symbionts has so far been investigated, at the molecular, genomic and metabolomics level, only in females, whereas the roles of microbiota in male reproduction are still unexplored. RESULTS:Here we begin unravelling the impact of microbiota on Glossina m. morsitans (G. morsitans) male reproductive biology by generating transcriptomes from the reproductive tissues of males deprived of their endosymbionts (aposymbiotic) via maternal antibiotic treatment and dietary supplementation. We then compared the transcriptional profiles of genes expressed in the male reproductive tract of normal and these aposymbiotic flies. We showed that microbiota removal impacts several male reproductive genes by depressing the activity of genes in the male accessory glands (MAGs), including sequences encoding seminal fluid proteins, and increasing expression of genes in the testes. In the MAGs, in particular, the expression of genes related to mating, immunity and seminal fluid components' synthesis is reduced. In the testes, the absence of symbionts activates genes involved in the metabolic apparatus at the basis of male reproduction, including sperm production, motility and function. CONCLUSIONS:Our findings mirrored the complementary roles male accessory glands and testes play in supporting male reproduction and open new avenues for disentangling the interplay between male insects and endosymbionts. From an applied perspective, unravelling the metabolic and functional relationships between tsetse symbionts and male reproductive physiology will provide fundamental information useful to understanding the biology underlying improved male reproductive success in tsetse. This information is of particular importance in the context of tsetse population control via Sterile Insect Technique (SIT) and its impact on trypanosomiasis transmission.

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How much does obesity affect the male reproductive function?

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How much does obesity affect the male reproductive function?

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