Is overweight a risk factor for reduced semen quality and altered serum sex hormone profile?

Aggerholm, Anette Skærbech; Thulstrup, Ane Marie; Toft, Gunnar; Ramlau‐Hansen, Cecilia Høst; Bonde, Jens Peter

doi:10.1016/j.fertnstert.2007.07.1292

Cited by 247 publications

(234 citation statements)

References 26 publications

Supporting

Mentioning

191

Contrasting

Unclassified

Order By: Relevance

“…Th ere was, however, strong evidence for a negative relationship between increased BMI and the levels of testosterone, sex hormone binding globulin (SHBG) and free testosterone 6 . Th ese results support the earlier fi ndings in a study on 2139 cases where overweight and obese men had a markedly changed sex hormone profi le in serum, whereas reduction of semen quality was marginal 7 . Similarly, no signifi cant correlation was found between BMI and semen parameters measured in a recently published cross-sectional study on 511 men 8 .…”

Section: Introductionsupporting

confidence: 89%

“…Th erefore, it seems that dysregulation of the hypothalamic-pituitary-gonadal (HPG) axis as a consequence of male obesity might further explain the increased risks of sperm disorders and infertility 7,[29][30][31] . Another key hormone produced by white adipose tissue is leptin the production of which increases with the amount of body fat and which plays a pivotal role in regulating the energy intake and expenditure.…”

Section: Th E Mechanisms Linking Obesity To Male Infertilitymentioning

confidence: 99%

“…Th e studies reporting correlations between obesity and fertility have generally been inconclusive because it remains unclear to what extent obesity aff ects the reproductive potential in men. In several studies, it has been suggested that overweight and obese men showed no signifi cantly increased relative risk of abnormal semen parameters [6][7][8] . A systematic review with meta-analysis of 31 studies on 6800 men revealed little association between increased body mass index (BMI), average sperm concentration and total sperm count.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Influence of Male Obesity on Fertility

Kasum

Anić-Jurica

Čehić

et al. 2016

ACC

View full text Add to dashboard Cite

SUMMARY -Th e aim of this review is to analyze current diagnostic approaches to obesity in adult men, the potential mechanisms linking obesity to infertility, and treatment options aimed at improving reproductive health. Obesity has become a worldwide epidemic with the estimated prevalence increasing from 28.8% to 36.9% between 1980 and 2013. In terms of diagnosis, numerous simple techniques have been developed including body mass index, waist to hip ratio, waist circumference, bioelectrical impedance analysis, ultrasound and skinfold measurements. Additionally, several other less available but more accurate techniques have been suggested, such as air displacement plethysmography, dual energy x-ray absorptiometry, computed tomography and magnetic resonance imaging. In addition to cardiovascular and other disorders, male obesity can negatively aff ect the male reproductive potential through abnormal reproductive hormone levels, reduced semen quality, increased release of adipose-derived hormones and adipokines, as well as thermal, genetic and sexual mechanisms. In the management of obesity related male infertility, natural weight loss is the cornerstone and regular exercise the fi rst-line treatment. Although bariatric surgery results in greater improvements in weight loss outcomes when compared to non-surgical interventions, further research is required to clarify its overall infl uence on male fertility.

show abstract

Section: Introductionsupporting

confidence: 89%

Section: Th E Mechanisms Linking Obesity To Male Infertilitymentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Influence of Male Obesity on Fertility

Kasum

Anić-Jurica

Čehić

et al. 2016

ACC

View full text Add to dashboard Cite

show abstract

“…Confusingly, Hammoud et al (2008b) initially reported that the incidence of oligo-and asthenozoospermia increased with increasing BMI, a finding seemingly contradicted by a subsequent critical review of the literature by the same group (Hammoud et al 2008a), which concluded that obesity had only a modest affect on male fertility. The latter view is supported by Aggerholm et al (2008) who found that semen quality from men with a BMI between 25 and 30 kg/m 2 was only marginally decreased if at all and by MacDonald et al (2010) who conducted a meta analysis of five published studies and concluded that there was little evidence of a relationship between BMI and semen quality. This disparity in concordance is reminiscent of studies on another co-morbidity of MetS, that of diabetes, where results on the condition's influence on sperm quantity and quality are also conflicting and inconclusive (Handelsman et al 1985, Vignon et al 1991, Niven et al 1995.…”

Section: Introductionmentioning

confidence: 95%

Spermatogenic and sperm quality differences in an experimental model of metabolic syndrome and hypogonadal hypogonadism

Mallidis¹,

Czerwiec²,

Filippi³

et al. 2011

Reproduction

View full text Add to dashboard Cite

The synergistic effect of the co-morbidities that comprise metabolic syndrome (MetS) is increasingly being recognised as an important contributor in the pathology of a broad spectrum of seemingly disparate conditions. However, in terms of male reproductive function, beyond erectile dysfunction, little is known about the influence of this cohort (collectively or separately) on spermatogenesis and sperm quality. The aims of this study were to assess the reproductive tract of a MetS animal model for detrimental changes, to determine whether a group of compounds (advanced glycation end products and their receptor) known to cause cell dysfunction and DNA damage was present and assess whether hypogonadotropic hypogonadism was the main contributing factor for the changes seen. Animals fed a high-fat diet were found to have significantly increased cholesterol, triglycerides, blood glucose, mean arterial pressure and visceral fat levels. Although serum testosterone was decreased, no changes were seen in either testicular or epididymal histology. Immunolocalisation of N 3 -carboxymethyl-lysine and the receptor for advanced glycation end products was found in the testes, epididymides and sperm of the two treated groups of animals; however, ELISA did not show any difference in protein levels. Similarly, assessment of sperm nuclear DNA (nDNA) fragmentation by acridine orange test did not find significant differences in nDNA integrity. We conclude that the minimal effect on spermatogenesis and sperm quality seen in our model is probably due to the moderate increase of blood glucose rather than the hypogonadism.

show abstract

“…More than one-third of men of reproductive age in the United States are classified as obese [1]. Paternal obesity not only impairs male fertility by impacting sperm count, motility and chromatin integrity [2][3][4][5][6][7] but also reduces subsequent embryo development, implantation rates, pregnancy success and live birth rates [8][9][10][11][12]. Interestingly metabolic syndrome, which includes obesity, in fathers is associated with polycystic ovary syndrome in daughters [13].…”

Section: Introductionmentioning

confidence: 99%

Female offspring sired by diet induced obese male mice display impaired blastocyst development with molecular alterations to their ovaries, oocytes and cumulus cells

Fullston

Shehadeh

Sandeman

et al. 2015

J Assist Reprod Genet

View full text Add to dashboard Cite

Purpose To investigate the impacts that a paternal high fat diet (HFD) has on embryology, ovarian/cumulus cell gene expression and COC metabolism from female offspring, using a mouse model. Methods Founder male mice were either fed a control diet (CD) or a HFD for 12 weeks. The HFD induced obesity but not diabetes, and founder males were then mated to normal weight CD fed female mice. Female offspring were maintained on a CD, super-ovulated, mated and the resultant zygotes were cultured to the blastocyst stage for embryo morphology, blastocyst cell number and apoptosis assessment. Ovaries and cumulus cells from offspring were collected for gene expression analysis of selected genes that maintain chromatin remodeling and endoplasmic reticulum (ER), metabolic and inflammatory homeostasis. Cumulus/oocyte complexes were also investigated for glucose uptake and lipid accumulation. Results Female offspring sired by obese fathers produced embryos with delayed development and impaired quality, displayed increases in ovarian expression of Glut1, Glut3 and Glut4, and an increase in cumulus cell expression of Glut4. Interestingly their COCs did take up more glucose, but did accumulate more lipid. Conclusions A paternal HFD is associated with subfertility in female offspring despite the offspring being fed a CD and this subfertility is concomitant with ovarian/cumulus cell molecular alterations and increased lipid accumulation.

show abstract

Is overweight a risk factor for reduced semen quality and altered serum sex hormone profile?

Cited by 247 publications

References 26 publications

Influence of Male Obesity on Fertility

Influence of Male Obesity on Fertility

Spermatogenic and sperm quality differences in an experimental model of metabolic syndrome and hypogonadal hypogonadism

Female offspring sired by diet induced obese male mice display impaired blastocyst development with molecular alterations to their ovaries, oocytes and cumulus cells

Contact Info

Product

Resources

About