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孕期和哺乳期母体营养不良会影响成年后代的睾丸形态、精子发生周期阶段和睾丸 IGF-I 系统。

Maternal undernutrition during pregnancy and lactation affects testicular morphology, the stages of spermatogenic cycle, and the testicular IGF-I system in adult offspring.

机构信息

Facultad de Veterinaria, Universidad de la República, Montevideo, Uruguay.

School of Agriculture and Environment, Faculty of Science, and UWA Institute of Agriculture, University of Western Australia, Perth, Australia.

出版信息

J Dev Orig Health Dis. 2020 Oct;11(5):473-483. doi: 10.1017/S2040174420000306. Epub 2020 Apr 28.

DOI:10.1017/S2040174420000306
PMID:32340648
Abstract

Maternal undernutrition decreases sperm production in male offspring, possibly through insulin-like growth factor (IGF-I). To test this hypothesis, we fed pregnant Wistar rats ad libitum with a standard diet (CONTROL) or fed 50% of CONTROL intake, either throughout pregnancy (UNP), lactation (UNL, or both (UNPL). After weaning, male offspring (n = 10 per treatment) were fed a standard diet until postnatal day 160, when testes process for histological and molecular analyses. IGF-I immunostaining area and intensity in the testis were greater (P = 0.003) in the UNPL group compared to CONTROL, but lower in the UNP group (P < 0.0001). Levels of IGF-I receptor transcript were lower in the UNPL and UNL groups, compared to CONTROL. There were more Ki-67-positive germ and Sertoli cells, in all underfed groups than in CONTROL. Compared to CONTROL, frequency of spermatogenic cycle stage VII was lower in all underfed groups, and seminiferous tubule diameter was smaller in UNP and UNPL. Plasma FSH concentrations were greater in UNP male offspring compared to all groups (P = 0.05), whereas inhibin B concentrations were greater in UNP (P = 0.01) and UNL (P = 0.003) than in CONTROL or UNPL. Thus, prenatal undernutrition leads to a decrease in testicular IGF-I levels, whereas of pre- and postnatal undernutrition increased testicular IGF-I levels and decreased amounts of IGF-I receptor mRNA in adult offspring. We conclude that maternal undernutrition during pregnancy and lactation leads to long-lasting effects on adult male offspring testicular morphology, spermatogenesis, and IGF-I testicular system.

摘要

母体营养不良会减少雄性后代的精子生成,这可能是通过胰岛素样生长因子(IGF-I)实现的。为了验证这一假说,我们让怀孕的 Wistar 大鼠自由摄取标准饮食(CONTROL)或 50%的 CONTROL 摄入量,无论是在怀孕期间(UNP)、哺乳期(UNL)还是两者兼而有之(UNPL)。断奶后,雄性后代(每组 10 只)喂食标准饮食,直至产后 160 天,此时对睾丸进行组织学和分子分析。与 CONTROL 相比,UNPL 组睾丸中 IGF-I 免疫染色面积和强度更大(P = 0.003),但 UNP 组更低(P < 0.0001)。与 CONTROL 相比,UNPL 和 UNL 组的 IGF-I 受体转录水平较低。与 CONTROL 相比,所有营养不良组的 Ki-67 阳性生殖细胞和支持细胞更多。与 CONTROL 相比,所有营养不良组的精子发生周期阶段 VII 的频率更低,UNP 和 UNPL 的精小管直径更小。与所有组相比,UNP 雄性后代的血浆 FSH 浓度更高(P = 0.05),而 UNP(P = 0.01)和 UNL(P = 0.003)的抑制素 B 浓度高于 CONTROL 或 UNPL。因此,产前营养不良会导致睾丸 IGF-I 水平降低,而产前和产后营养不良会导致成年雄性后代睾丸形态、精子发生和 IGF-I 睾丸系统的 IGF-I 受体 mRNA 减少。我们得出结论,妊娠和哺乳期的母体营养不良会对雄性后代睾丸形态、精子发生和 IGF-I 睾丸系统产生长期影响。

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