scholarly journals Perinatal Propylthiouracil-Induced Hypothyroidism Impaired Motor Coordination in Adult Female Offspring

2019 ◽  
Vol 4 (3) ◽  
Author(s):  
Miski A. Khairinisa ◽  
Yusuke Takatsuru ◽  
Izuki Amano ◽  
Michifumi Kokubo ◽  
Asahi Haijima ◽  
...  

Thyroid hormone (TH) play crucial roles in the growth and development of brain. Efficiency of TH during the perinatal period results in severe mental and physical retardation, known as cretinism in humans. Animal models have largely focused on mild and severe hypothyroidism associated with deficits in body weight, developmental delays, and cognitive deficits. Although various behavioral analyses have been reported, the effect of perinatal hypothyroidism in adult female mice has not been clarified. The aim of this study was to examine whether propylthiouracil (PTU)-induced hypothyroidism could impair motor coordination in female offspring. We used C57BL/6j mice and divided them into three groups based on the dose of PTU which was applied during perinatal period (embryonic day-14 to postnatal day-14); control, 5 ppm, and 50 ppm groups. We observed motor coordination function and additional nociceptive test in female offspring. We found that motor coordination and nociceptive threshold were affected in 50 ppm groups. We concluded that the moderate hypothyroidism could impair motor coordination in adult offspring.

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Meng Zuo ◽  
Guotao Liao ◽  
Wenqian Zhang ◽  
Dan Xu ◽  
Juan Lu ◽  
...  

Abstract Objective PCOS is a heterogeneous endocrine disorder with both reproductive and metabolic abnormalities. At present, PCOS has been confirmed to have a certain genetic background. Compared with healthy women, the vast majority of PCOS patients have hyperandrogenemia, and this excessive androgen exposure during pregnancy may affect the development of female fetuses. The aim of the current study was to investigate the effect of adiponectin intervention during early pregnancy of obese mice with PCOS on the metabolic phenotype of adult female offspring. Methods After the PCOS model was established, C57BL/6J mice were divided into maternal-control, maternal-PCOS, and maternal-PCOS + APN groups. DHEA-induced PCOS mice were supplemented with adiponectin (10 mg/kg/day) in the early pregnancy in order to eliminate adverse hormone exposure and then traced for endocrine indicators in their adult female offspring, which were observed for metabolism syndrome or endocrine disturbance and exhibited the main effects of APN. To further explore the underlying mechanism, the relative expressions of phosphorylated AMPK, PI3K, and Akt were detected in the ovaries of offspring mice. Results The serum testosterone level of the maternal-PCOS + APN group in early pregnancy was significantly lower than that of the maternal-PCOS group (p < 0.01). The serum testosterone level in the offspring-PCOS + APN group was significantly lower than in the offspring-PCOS group (p <0.05), the diestrus time characterized by massive granulocyte aggregation in the estrus cycle was significantly shorter than in the offspring-PCOS group (p<0.05), and the phenotypes of PCOS-like reproductive disorders and metabolic disorders, such as obesity, insulin resistance, impaired glucose tolerance, and hyperlipidemia, were also significantly improved in the offspring-PCOS + APN group (p < 0.05). Compared with the control group, the expression levels of phosphorylated AMPK, PI3K, and Akt in the offspring-PCOS group were significantly decreased (p < 0.05), while those in the offspring-PCOS + APN group were significantly increased (p < 0.05). Conclusions APN intervention in early pregnancy significantly reduced the adverse effects of maternal obesity and high androgen levels during pregnancy on female offspring and corrected the PCOS-like endocrine phenotype and metabolic disorders of adult female offspring. This effect may be caused by the activation of the AMPK/PI3K-Akt signaling pathway in PCOS offspring mice.


2012 ◽  
Vol 303 (11) ◽  
pp. E1373-E1385 ◽  
Author(s):  
Miao Sun ◽  
Manuel Maliqueo ◽  
Anna Benrick ◽  
Julia Johansson ◽  
Ruijin Shao ◽  
...  

Here, we tested the hypothesis that excess maternal androgen in late pregnancy reduces placental and fetal growth, increases placental steroidogenesis, and adversely affects glucose and lipid metabolism in adult female offspring. Pregnant Wistar rats were randomly assigned to treatment with testosterone (daily injections of 5 mg of free testosterone from gestational days 16 to 19) or vehicle alone. In experiment 1, fetal and placental weights, circulating maternal testosterone, estradiol, and corticosterone levels, and placental protein expression and distribution of estrogen receptor-α and -β, androgen receptor, and 17β-hydroxysteroid dehydrogenase 2 were determined. In experiment 2, birth weights, postnatal growth rates, circulating testosterone, estradiol, and corticosterone levels, insulin sensitivity, adipocyte size, lipid profiles, and the presence of nonalcoholic fatty liver were assessed in female adult offspring. Treatment with testosterone reduced placental and fetal weights and increased placental expression of all four proteins. The offspring of testosterone-treated dams were born with intrauterine growth restriction; however, at 6 wk of age there was no difference in body weight between the offspring of testosterone- and control-treated rats. At 10–11 wk of age, the offspring of the testosterone-treated dams had less fat mass and smaller adipocyte size than those born to control rats and had no difference in insulin sensitivity. Circulating triglyceride levels were higher in the offspring of testosterone-treated dams, and they developed nonalcoholic fatty liver as adults. We demonstrate for the first time that prenatal testosterone exposure alters placental steroidogenesis and leads to dysregulation of lipid metabolism in their adult female offspring.


2020 ◽  
Vol 16 (72) ◽  
pp. 706
Author(s):  
Hasnah Bahari ◽  
AzrinaZainal Abidin ◽  
SanthraSegaran Balan ◽  
KokilaVani Perumal ◽  
NurainSyahirah Rosli ◽  
...  

2018 ◽  
Vol 110 (4) ◽  
pp. e53
Author(s):  
A. Eubanks ◽  
S. Mumford ◽  
M.J. Hill ◽  
A.H. DeCherney ◽  
K. Kim ◽  
...  

2010 ◽  
Vol 21 (4) ◽  
pp. 283-291 ◽  
Author(s):  
Chengjun Yu ◽  
Fadao Tai ◽  
Ruiyong Wu ◽  
Zhenzhen Song ◽  
Xia Zhang ◽  
...  

1984 ◽  
Vol 11 (1) ◽  
pp. 21 ◽  
Author(s):  
JC Merchant ◽  
K Newgrain ◽  
B Green

The growth and development, from 10 to 270 days old, of eastern quolls in a captive colony was recorded. Young were able to detach from the teat by 65 days of age and their eyes were open by 80 days. Statistically significant differences in some measurements from males and females were found as early as 85 days of age. The weaning period commenced at 102 days ofage, and coincided with eruption ofthe first molar teeth. Total independence, determined by the cessation of lactation in the mother, was as early as 142 days in litters of one or as late as 200 days in larger litters. There was a high correlation between litter size and age at independence. Lactation was maintained in all previously suckled mammary glands of adult females after the death of young aged 65 days or over if some siblings remained. This was due to the ability of young of this age to detach and reattach to the teats at will. The implication of this observation is that the commonly held view that the numbers of surviving young in marsupial litters corresponds to the number of lactating teats in the adult female may not always be correct.


Author(s):  
Wen-Chung Liu ◽  
Chih-Wei Wu ◽  
Pi-Lien Hung ◽  
Julie Y. H. Chan ◽  
You-Lin Tain ◽  
...  

Maternal high-fructose diets (HFD) impair the learning and memory capacity of adult female offspring via histone deacetylase 4 (HDAC4). Hippocampal adult neurogenesis is important for supporting the function of existing neural circuits. In this study, we investigated the effects of maternal HFD on hippocampal neural stem cell (NSC) proliferation and neuronal differentiation in adult offspring. Increased nuclear HDAC4 enzyme activity was detected in the hippocampus of HFD female offspring. The Western blot analyses indicated that the expressions of sex-determining region Y box2 (SOX2) and the transcription factor Paired Box 6 (PAX6), which are critical for the progression of NSC proliferation and differentiation, were downregulated. Concurrently, the expression of Ki67 (a cellular marker for proliferation) and doublecortin (DCX), which are related to NSC division and neuronal differentiation, was suppressed. Intracerebroventricular infusion with class II HDAC inhibitor (Mc1568, 4 weeks) led to the upregulation of these proteins. Environmental stimulation reversed the expression of Ki67 and DCX and the counts of Ki67- and DCX-positive cells in the hippocampi of HFD offspring as a result of providing the enriched housing for 4 weeks. Together, these results demonstrate that the suppressive effects of maternal HFD on hippocampal NSC proliferation and neuronal differentiation are reversibly mediated through HDAC4 and can be effectively reversed by environmental stimulation. The advantageous effects of environmental enrichment were possibly mediated by HDAC4 suppression.


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