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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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Description of an obese mouse model established after 10 weeks on HFD.(A) Representative picture of 15-week old obese and control mice. (B) Comparison of time-dependent increases in body weight between CD (n = 27) and HFD groups (n = 30). (C) Weekly food consumption by mice in CD and HFD groups. (D) Hematoxylin and eosin-stained hepatic sections from mice both fed control diet (CD) and high-fat diet (HFD). (D2) and (D4) are two-fold enlarged views of (D1) and (D3). Scale bars = 50 μm. Data are expressed as mean ± SEM. * P<0.05, ** P<0.01.
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pone.0120775.g001: Description of an obese mouse model established after 10 weeks on HFD.(A) Representative picture of 15-week old obese and control mice. (B) Comparison of time-dependent increases in body weight between CD (n = 27) and HFD groups (n = 30). (C) Weekly food consumption by mice in CD and HFD groups. (D) Hematoxylin and eosin-stained hepatic sections from mice both fed control diet (CD) and high-fat diet (HFD). (D2) and (D4) are two-fold enlarged views of (D1) and (D3). Scale bars = 50 μm. Data are expressed as mean ± SEM. * P<0.05, ** P<0.01.

Mentions: Male C57BL/6 mice fed a high-fat diet for 10 weeks gained significantly more body weight than their age-matched littermates fed a normal diet (33.54 ± 0.81 vs. 29.02 ± 0.38, n = 30, P<0.01). The difference in body weight between these two groups became significant after 3 weeks being fed their designated diets and persisted for the subsequent seven weeks as shown in Fig 1A and 1B. The feed intake per week (g/week) of the HFD group was always less than that of the CD group (Fig 1C). However, the high-fat diet had a much higher caloric content than the normal diet.


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)

Description of an obese mouse model established after 10 weeks on HFD.(A) Representative picture of 15-week old obese and control mice. (B) Comparison of time-dependent increases in body weight between CD (n = 27) and HFD groups (n = 30). (C) Weekly food consumption by mice in CD and HFD groups. (D) Hematoxylin and eosin-stained hepatic sections from mice both fed control diet (CD) and high-fat diet (HFD). (D2) and (D4) are two-fold enlarged views of (D1) and (D3). Scale bars = 50 μm. Data are expressed as mean ± SEM. * P<0.05, ** P<0.01.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4401673&req=5

pone.0120775.g001: Description of an obese mouse model established after 10 weeks on HFD.(A) Representative picture of 15-week old obese and control mice. (B) Comparison of time-dependent increases in body weight between CD (n = 27) and HFD groups (n = 30). (C) Weekly food consumption by mice in CD and HFD groups. (D) Hematoxylin and eosin-stained hepatic sections from mice both fed control diet (CD) and high-fat diet (HFD). (D2) and (D4) are two-fold enlarged views of (D1) and (D3). Scale bars = 50 μm. Data are expressed as mean ± SEM. * P<0.05, ** P<0.01.
Mentions: Male C57BL/6 mice fed a high-fat diet for 10 weeks gained significantly more body weight than their age-matched littermates fed a normal diet (33.54 ± 0.81 vs. 29.02 ± 0.38, n = 30, P<0.01). The difference in body weight between these two groups became significant after 3 weeks being fed their designated diets and persisted for the subsequent seven weeks as shown in Fig 1A and 1B. The feed intake per week (g/week) of the HFD group was always less than that of the CD group (Fig 1C). However, the high-fat diet had a much higher caloric content than the normal diet.

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