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Diet-induced obesity in male C57BL/6 mice decreases fertility as a consequence of disrupted blood-testis barrier.

Fan Y, Liu Y, Xue K, Gu G, Fan W, Xu Y, Ding Z - PLoS ONE (2015)

Bottom Line: The results clearly show that the percentage of sperm motility and progressive motility significantly decreased, whereas the proportion of teratozoospermia dramatically increased in HFD mice compared to those in normal diet fed controls.Moreover, testicular morphological analyses revealed that seminiferous epithelia were severely atrophic, and cell adhesions between spermatogenic cells and Sertoli cells were loosely arranged in HFD mice.Meanwhile, the integrity of the blood-testis barrier was severely interrupted consistent with declines in the tight junction related proteins, occludin, ZO-1 and androgen receptor, but instead endocytic vesicle-associated protein, clathrin rose.

View Article: PubMed Central - PubMed

Affiliation: Department of Human Anatomy, Histology and Embryology, School of Medicine, Shanghai Jiao Tong University, Shanghai Key Laboratory for Reproductive Medicine, Shanghai, China.

ABSTRACT
Obesity is a complex metabolic disease that is a serious detriment to both children and adult health, which induces a variety of diseases, such as cardiovascular disease, type II diabetes, hypertension and cancer. Although adverse effects of obesity on female reproduction or oocyte development have been well recognized, its harmfulness to male fertility is still unclear because of reported conflicting results. The aim of this study was to determine whether diet-induced obesity impairs male fertility and furthermore to uncover its underlying mechanisms. Thus, male C57BL/6 mice fed a high-fat diet (HFD) for 10 weeks served as a model of diet-induced obesity. The results clearly show that the percentage of sperm motility and progressive motility significantly decreased, whereas the proportion of teratozoospermia dramatically increased in HFD mice compared to those in normal diet fed controls. Besides, the sperm acrosome reaction fell accompanied by a decline in testosterone level and an increase in estradiol level in the HFD group. This alteration of sperm function parameters strongly indicated that the fertility of HFD mice was indeed impaired, which was also validated by a low pregnancy rate in their mated normal female. Moreover, testicular morphological analyses revealed that seminiferous epithelia were severely atrophic, and cell adhesions between spermatogenic cells and Sertoli cells were loosely arranged in HFD mice. Meanwhile, the integrity of the blood-testis barrier was severely interrupted consistent with declines in the tight junction related proteins, occludin, ZO-1 and androgen receptor, but instead endocytic vesicle-associated protein, clathrin rose. Taken together, obesity can impair male fertility through declines in the sperm function parameters, sex hormone level, whereas during spermatogenesis damage to the blood-testis barrier (BTB) integrity may be one of the crucial underlying factors accounting for this change.

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Comparison of sperm function parameters in mice fed either CD or HFD.(A) Sperm motility in mice fed either CD or HFD analyzed by CASA. (B) Sperm progressive motility in mice fed either CD or HFD analyzed by CASA. (C) Sperm concentration from cauda epididymis in mice fed either CD or HFD analyzed by CASA. (D) Sperm morphology analysis of CD-fed mice (D1) and HFD-fed mice (D2) using Diff-Quick method. Arrows indicate abnormal spermatozoa. Scale bar = 50 μm. (D3) Normal and abnormal spermatozoa in different forms, Scale bar = 10 μm. (D4) Comparison of sperm abnormality in mice fed either HFD or CD. Data are expressed as mean ± SEM. *P<0.05, **P<0.01.
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pone.0120775.g003: Comparison of sperm function parameters in mice fed either CD or HFD.(A) Sperm motility in mice fed either CD or HFD analyzed by CASA. (B) Sperm progressive motility in mice fed either CD or HFD analyzed by CASA. (C) Sperm concentration from cauda epididymis in mice fed either CD or HFD analyzed by CASA. (D) Sperm morphology analysis of CD-fed mice (D1) and HFD-fed mice (D2) using Diff-Quick method. Arrows indicate abnormal spermatozoa. Scale bar = 50 μm. (D3) Normal and abnormal spermatozoa in different forms, Scale bar = 10 μm. (D4) Comparison of sperm abnormality in mice fed either HFD or CD. Data are expressed as mean ± SEM. *P<0.05, **P<0.01.

Mentions: CASA analysis of spermatozoa extracted from the cauda epididymides revealed that the percentage of motility and progressive motility significantly decreased in the HFD group when compared to those in the CD group (percentage of motility: 43.85 ± 2.35 vs. 53.27 ± 3.06; progressive motility: 15.82 ± 1.19 vs. 22.32 ± 1.67, n = 27, P<0.05) (Fig 3A and 3B). However, sperm concentration of HFD group was not significantly altered in comparison to that in the CD group (26.65 ± 4.18 vs. 28.83 ± 3.84, n = 27, P>0.05) (Fig 3C). Moreover, we also observed that there was a higher ratio of teratozoospermia in the HFD group compared to that in the CD group (Fig 3D1–3D4; 28.17 ± 1.64 vs. 18.17 ± 1.74, n = 3, P<0.05).


Diet-induced obesity in male C57BL/6 mice decreases fertility as a consequence of disrupted blood-testis barrier.

Fan Y, Liu Y, Xue K, Gu G, Fan W, Xu Y, Ding Z - PLoS ONE (2015)

Comparison of sperm function parameters in mice fed either CD or HFD.(A) Sperm motility in mice fed either CD or HFD analyzed by CASA. (B) Sperm progressive motility in mice fed either CD or HFD analyzed by CASA. (C) Sperm concentration from cauda epididymis in mice fed either CD or HFD analyzed by CASA. (D) Sperm morphology analysis of CD-fed mice (D1) and HFD-fed mice (D2) using Diff-Quick method. Arrows indicate abnormal spermatozoa. Scale bar = 50 μm. (D3) Normal and abnormal spermatozoa in different forms, Scale bar = 10 μm. (D4) Comparison of sperm abnormality in mice fed either HFD or CD. Data are expressed as mean ± SEM. *P<0.05, **P<0.01.
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Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4401673&req=5

pone.0120775.g003: Comparison of sperm function parameters in mice fed either CD or HFD.(A) Sperm motility in mice fed either CD or HFD analyzed by CASA. (B) Sperm progressive motility in mice fed either CD or HFD analyzed by CASA. (C) Sperm concentration from cauda epididymis in mice fed either CD or HFD analyzed by CASA. (D) Sperm morphology analysis of CD-fed mice (D1) and HFD-fed mice (D2) using Diff-Quick method. Arrows indicate abnormal spermatozoa. Scale bar = 50 μm. (D3) Normal and abnormal spermatozoa in different forms, Scale bar = 10 μm. (D4) Comparison of sperm abnormality in mice fed either HFD or CD. Data are expressed as mean ± SEM. *P<0.05, **P<0.01.
Mentions: CASA analysis of spermatozoa extracted from the cauda epididymides revealed that the percentage of motility and progressive motility significantly decreased in the HFD group when compared to those in the CD group (percentage of motility: 43.85 ± 2.35 vs. 53.27 ± 3.06; progressive motility: 15.82 ± 1.19 vs. 22.32 ± 1.67, n = 27, P<0.05) (Fig 3A and 3B). However, sperm concentration of HFD group was not significantly altered in comparison to that in the CD group (26.65 ± 4.18 vs. 28.83 ± 3.84, n = 27, P>0.05) (Fig 3C). Moreover, we also observed that there was a higher ratio of teratozoospermia in the HFD group compared to that in the CD group (Fig 3D1–3D4; 28.17 ± 1.64 vs. 18.17 ± 1.74, n = 3, P<0.05).

Bottom Line: The results clearly show that the percentage of sperm motility and progressive motility significantly decreased, whereas the proportion of teratozoospermia dramatically increased in HFD mice compared to those in normal diet fed controls.Moreover, testicular morphological analyses revealed that seminiferous epithelia were severely atrophic, and cell adhesions between spermatogenic cells and Sertoli cells were loosely arranged in HFD mice.Meanwhile, the integrity of the blood-testis barrier was severely interrupted consistent with declines in the tight junction related proteins, occludin, ZO-1 and androgen receptor, but instead endocytic vesicle-associated protein, clathrin rose.

View Article: PubMed Central - PubMed

Affiliation: Department of Human Anatomy, Histology and Embryology, School of Medicine, Shanghai Jiao Tong University, Shanghai Key Laboratory for Reproductive Medicine, Shanghai, China.

ABSTRACT
Obesity is a complex metabolic disease that is a serious detriment to both children and adult health, which induces a variety of diseases, such as cardiovascular disease, type II diabetes, hypertension and cancer. Although adverse effects of obesity on female reproduction or oocyte development have been well recognized, its harmfulness to male fertility is still unclear because of reported conflicting results. The aim of this study was to determine whether diet-induced obesity impairs male fertility and furthermore to uncover its underlying mechanisms. Thus, male C57BL/6 mice fed a high-fat diet (HFD) for 10 weeks served as a model of diet-induced obesity. The results clearly show that the percentage of sperm motility and progressive motility significantly decreased, whereas the proportion of teratozoospermia dramatically increased in HFD mice compared to those in normal diet fed controls. Besides, the sperm acrosome reaction fell accompanied by a decline in testosterone level and an increase in estradiol level in the HFD group. This alteration of sperm function parameters strongly indicated that the fertility of HFD mice was indeed impaired, which was also validated by a low pregnancy rate in their mated normal female. Moreover, testicular morphological analyses revealed that seminiferous epithelia were severely atrophic, and cell adhesions between spermatogenic cells and Sertoli cells were loosely arranged in HFD mice. Meanwhile, the integrity of the blood-testis barrier was severely interrupted consistent with declines in the tight junction related proteins, occludin, ZO-1 and androgen receptor, but instead endocytic vesicle-associated protein, clathrin rose. Taken together, obesity can impair male fertility through declines in the sperm function parameters, sex hormone level, whereas during spermatogenesis damage to the blood-testis barrier (BTB) integrity may be one of the crucial underlying factors accounting for this change.

Show MeSH
Related in: MedlinePlus