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. 2017 Oct 26:27:20.
doi: 10.1186/s12610-017-0064-9. eCollection 2017.

Paternal obesity: how bad is it for sperm quality and progeny health?

Affiliations

Paternal obesity: how bad is it for sperm quality and progeny health?

Georges Raad et al. Basic Clin Androl. .

Abstract

There is substantial evidence that paternal obesity is associated not only with an increased incidence of infertility, but also with an increased risk of metabolic disturbance in adult offspring. Apparently, several mechanisms may contribute to the sperm quality alterations associated with paternal obesity, such as physiological/hormonal alterations, oxidative stress, and epigenetic alterations. Along these lines, modifications of hormonal profiles namely reduced androgen levels and elevated estrogen levels, were found associated with lower sperm concentration and seminal volume. Additionally, oxidative stress in testis may induce an increase of the percentage of sperm with DNA fragmentation. The latter, relate to other peculiarities such as alteration of the embryonic development, increased risk of miscarriage, and development of chronic morbidity in the offspring, including childhood cancers. Undoubtedly, epigenetic alterations (ie, DNA methylation, chromatin modifications, and small RNA deregulation) of sperm related to paternal obesity and their consequences on the progeny are poorly understood determinants of paternal obesity-induced transmission. In this review, we summarize and discuss the data available in the literature regarding the biological, physiological, and molecular consequences of paternal obesity on male fertility potential and ultimately progeny health.

De plus en plus de données tendent à montrer que l’obésité paternelle a non seulement des effets néfastes sur la santé métabolique et reproductive de l’individu mais également sur celle de sa descendance. Les mécanismes mis en jeu dans ce processus incluraient des altérations physiologiques et hormonales des fonctions reproductives de l’homme obèse ainsi que des altérations épigénétiques au niveau du génome spermatique. Les modifications hormonales associées à l’obésité et qui se caractérisent principalement par une réduction du taux d’androgènes et une augmentation du niveau d’estrogène induiraient une altération des paramètres spermatiques, une diminution de la concentration ou de la numération totale en spermatozoïde et du volume séminal. Le stress oxydatif dans le testicule induirait une augmentation de la fragmentation de l’ADN spermatique et pourrait rendre compte de l’augmentation des risques de fausses-couches, des problèmes de développement embryonnaire ainsi que de l’augmentation des risques de mortalité chez la descendance, problèmes fréquemment rencontrés lorsque le père est. obèse. Les modifications épigénétiques (altérations des profils de méthylation de l’ADN, de la structure de la chromatine ou/et des profils d’expression des ARN spermatiques) induites par l’obésité sont, quant à elles, loin d’être comprises, même si elles sont, surement, les vecteurs clés de la transmission épigénétique paternelle des maladies métaboliques. L’objet de cette revue est. de résumer puis de discuter les différentes études expérimentales et épidémiologiques publiés à ce jour sur les conséquences physiologiques et moléculaire de l’obésité paternelle sur la santé de l’individu et sur celle de sa descendance.

Keywords: Epigenetics; Fertility; Inheritance; Obesity; Small RNAs.

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The authors declare that they have no competing interests.

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Figures

Fig. 1
Fig. 1
Illustration of testicular interstitial tissue in normal weight men (a) and obese men (b). Spz = Spermatozoa; sc = Sertoli cells; PT = peritubular cells; B.M. = basement membrane. TNF-alpha: Tumor necrosis factor alpha; MCP-1 = monocyte chemoattractant protein-1; F4/80: a defining marker of murine macrophage populations
Fig. 2
Fig. 2
Schematic representation of the hypothalamic pituitary testicular axis and hormone testicular production upon obesity. Solid lines represent the hormonal regulation in normal weight men; dashed lines represent the inhibitory effects of obesity. AMH: anti-müllerien hormone; ABP: androgen binding protein; E2: oestrogen; FSH: follicle stimulating hormone; GnRH: gonadotropin releasing hormone; LH: luteinizing hormone; LHR: luteinizing hormone receptor; SHBG: sex hormone binding globulin; StAR: steroidogenic acute regulatory protein

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