Intrauterine Hyponutrition Reduces Fetal Testosterone Production and Postnatal Sperm Count in the Mouse.
Intrauterine Hyponutrition Reduces Fetal Testosterone Production and Postnatal Sperm Count in the Mouse.
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宫内不足会减少小鼠中胎儿睾丸激素的产生和产后精子数。
DOI：
10.1210/jendso/bvac022
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发表时间：
2022-04-01
影响因子：
4.1
通讯作者：
Ogata T
中科院分区：
文献类型：
--
作者：
Fujisawa Y;Ono H;Konno A;Yao I;Itoh H;Baba T;Morohashi K;Katoh-Fukui Y;Miyado M;Fukami M;Ogata T
尽管宫内低营养素被认为是人类“睾丸发育不全综合征”（TDS）发展的危险因素，但其潜在机制仍不清楚。为了阐明潜在的机制，我们在整个妊娠过程中，给阴道塞阳性的C57 BL/6 N雌性小鼠随意喂食常规食物（对照雌性）（C-雌性）或从6.5 dpc开始C-雌性平均每日摄入量的50%（限制热量的女性）（R-雌性），并比较了从C-雌性小鼠分娩的17.5-dpc-龄雄性小鼠之间的雄性生殖结果（C-胎儿）和从R-雌性（R-胎儿）分娩的那些以及由C-雌性（C-后代）所生的6周龄雄性小鼠和由R-雌性（R-后代）所生的6周龄雄性小鼠之间。 与C-胎儿相比，R-胎儿（1）外生殖器形态正常，肛门生殖器距离指数显著降低，（2）睾丸组成细胞数量正常，（3）睾丸内睾酮显著降低，与类固醇生成基因表达显著降低相关。此外，与C-后代相比，R-后代具有（1）显著增加的TUNEL阳性细胞和其他睾丸组成细胞的正常数量，（2）正常的睾丸内睾酮，与类固醇生成基因的正常表达相关，（3）显著减少的精子数，以及正常的睾丸重量和精子活力，和（4）显著改变的氧化应激相关的表达，睾丸发育相关基因和精子发生相关基因。 结果，连同以前的数据，包括睾酮剥夺和氧化应激诱发的细胞凋亡激活之间的关联，意味着胎儿睾酮的生产减少是宫内低营养胎儿TDS发展的主要潜在因素，TDS包括在健康和疾病的发展起源的临床谱。
Although intrauterine hyponutrition is regarded as a risk factor for the development of “testicular dysgenesis syndrome” (TDS) in the human, underlying mechanism(s) remain largely unknown. To clarify the underlying mechanism(s), we fed vaginal plug-positive C57BL/6N female mice with regular food ad libitum throughout the pregnant course (control females) (C-females) or with 50% of the mean daily intake of the C-females from 6.5 dpc (calorie-restricted females) (R-females), and compared male reproductive findings between 17.5-dpc-old male mice delivered from C-females (C-fetuses) and those delivered from R-females (R-fetuses) and between 6-week-old male mice born to C-females (C-offspring) and those born to R-females (R-offspring). Compared with the C-fetuses, the R-fetuses had (1) morphologically normal external genitalia with significantly reduced anogenital distance index, (2) normal numbers of testicular component cells, and (3) significantly low intratesticular testosterone, in association with significantly reduced expressions of steroidogenic genes. Furthermore, compared with the C-offspring, the R-offspring had (1) significantly increased TUNEL-positive cells and normal numbers of other testicular component cells, (2) normal intratesticular testosterone, in association with normal expressions of steroidogenic genes, (3) significantly reduced sperm count, and normal testis weight and sperm motility, and (4) significantly altered expressions of oxidation stress-related, apoptosis-related, and spermatogenesis-related genes. The results, together with the previous data including the association between testosterone deprivation and oxidative stress-evoked apoptotic activation, imply that reduced fetal testosterone production is the primary underlying factor for the development of TDS in intrauterine hyponutrition, and that TDS is included in the clinical spectrum of Developmental Origins of Health and Disease.
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影响因子：
5.9
作者：
Baba T;Otake H;Inoue M;Sato T;Ishihara Y;Moon JY;Tsuchiya M;Miyabayashi K;Ogawa H;Shima Y;Wang L;Sato R;Yamazaki T;Suyama M;Nomura M;Choi MH;Ohkawa Y;Morohashi KI
通讯作者：
Morohashi KI
影响因子：
2.9
作者：
Baskin, Laurence;Shen, Joel;Cunha, Gerald R.
通讯作者：
Cunha, Gerald R.
DOI：
10.1073/pnas.1002178107
发表时间：
2010-08-31
影响因子：
11.1
作者：
Kuroda, Junya;Ago, Tetsuro;Sadoshima, Junichi
通讯作者：
Sadoshima, Junichi
DOI：
10.1016/j.bbrc.2006.01.058
发表时间：
2006-03-24
影响因子：
3.1
作者：
Futchiyah;Zubair, M;Morohashi, K
通讯作者：
Morohashi, K
影响因子：
3.3
作者：
Gallavan, RH;Holson, JF;Reynolds, VL
通讯作者：
Reynolds, VL