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Journal articles on the topic 'Mice Reproduction'
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1
Lafaille, Marie, Patrick Gouat, and Christophe Féron. "Efficiency of delayed reproduction in Mus spicilegus." Reproduction, Fertility and Development 27, no. 3 (2015): 491. http://dx.doi.org/10.1071/rd13130.
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To cope with seasonally varying ecological constraints, some mammals temporally suppress breeding or delay their first reproduction. In field conditions, mound-building mice (Mus spicilegus) born in spring begin to reproduce when 2–3 months old, whereas individuals born at the end of summer delay their first reproduction for 6–8 months until the following spring. In order to test age effects on reproductive performance in M. spicilegus, sexually naïve mice were paired when 2–3 months old or at 6–8 months of age, and surveyed for reproduction. We show here that under laboratory conditions the aging of these mice does not impair their reproductive efficiency. Thus, the hypothesis of a lower reproductive potential in these relatively aged females seems to be contradicted. More surprisingly, the latency from pairing to the first reproduction was greater in the 2–3-month-old adults than in the delayed reproducers (6–8-month-old mice). Mound-building mice that are old enough to have overwintered do not suffer significant reproductive declines, but appear to reproduce as well and more quickly than younger first-time breeders.
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Munger, James C., and William H. Karasov. "Sublethal parasites in white-footed mice: impact on survival and reproduction." Canadian Journal of Zoology 69, no. 2 (February 1, 1991): 398–404. http://dx.doi.org/10.1139/z91-062.
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The potential impact of two parasites on the population density of host white-footed mice (Peromyscus leucopus) was assessed by measuring effects on survival and reproduction in field populations. Thirty-eight mice infected with larvae of the bot fly Cuterebra angustifrons had their larvae removed, another 41 mice remained infected, and 46 other mice were naturally uninfected during the experiment. No effect of bot larvae removal was detected on either survival (measured as attrition) or reproduction (measured as end of reproductive season). However, contrary to expectation, naturally infected mice had lower attrition and a marginally longer reproductive season than naturally uninfected mice. This latter result is probably an artifact, due to underlying differences between naturally infected and uninfected mice. Sixty-seven mice were experimentally infected with the tapeworm Hymenolepis citelli (64 mice were controls), but no effect was detected on attrition from the trappable population nor on the cessation of the reproductive season. Our results indicate that (i) these parasites are unlikely to have any effect on population density of white-footed mice, and (ii) it is potentially misleading to use "natural experiments" (comparison of naturally infected hosts with uninfected hosts) to study the impact of parasitic infection.
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Harini, C., S. B. Sainath, and P. Sreenivasula Reddy. "Recovery of suppressed male reproduction in mice exposed to progesterone during embryonic development by testosterone." REPRODUCTION 137, no. 3 (March 2009): 439–48. http://dx.doi.org/10.1530/rep-08-0438.
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The present study aimed to examine whether transplacental exposure to progesterone caused male reproductive abnormalities and whether the changes can be reversed after testosterone administration. Progesterone was injected to mice on day 1, 3, and 7 of pregnancy. The male pups (F1 generation) were allowed to grow for 50 days and assessed for reproductive performance. Gestational exposure to progesterone (7 mg/kg body weight) resulted in significant body weight gain with a decrease in reproductive tissue indices in mice. Total sperm count, viable sperm, and motile sperm decreased in experimental mice. Hypo-osmotic swelling test revealed that experimental mice sperm membrane integrity was severely altered. The activity levels of testicular steroidogenic marker enzymes (hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase cluster (HSD3B) and hydroxysteroid (17-beta) dehydrogenase 1 (HSD17B)) decreased significantly in mice exposed to progesterone during embryonic development when compared with the controls. The levels of serum testosterone decreased with an increase in serum FSH and LH in mice exposed to progesterone during embryonic development. Prenatal exposure to progesterone caused significant reduction in the number of spermatozoa and increase in the lumen of seminiferous tubule. The experimental mice that cohabited with normal females showed fertility reduction. Administration of testosterone (4.16 mg/kg body weight) on postnatal day 20, 30, and 40 to progesterone-exposed prenates resulted in recovery of progesterone-induced suppressed male reproduction. It is suggested that the impairment of male reproduction in mice exposed to progesterone during embryonic development could be mediated through the inhibition of testosterone production. These results also indicate thatin uteroexposure to progesterone affects male reproduction and that supplementation of testosterone restores the suppressed male reproduction.
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Rollo, C. D., J. Rintoul, and L. J. Kajiura. "Lifetime reproduction of giant transgenic mice: the energy stress paradigm." Canadian Journal of Zoology 75, no. 8 (August 1, 1997): 1336–45. http://dx.doi.org/10.1139/z97-758.
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Lifetime reproduction of female transgenic rat growth hormone (TRrGH) mice and their normal siblings was evaluated on a high-protein (38%) diet, a standard diet (23% protein), and the standard diet supplemented with sucrose cubes. Compared with those on the standard diet, normal mice fed the high-protein diet showed significant increases in litter size, number of litters, and lifetime fecundity. Number of litters and lifetime fecundity were also enhanced in normal mice fed sucrose. TRrGH mice showed no significant improvements in reproduction on the high-protein diet, but they were significantly smaller. Sucrose dramatically improved reproduction of TRrGH mice, with no reduction in mature mass. The percentage of fertile TRrGH mice increased from 45% on standard chow to 71% with sucrose. The number and size of litters of TRrGH mice also significantly increased with sucrose, mean lifetime fecundity doubling from 9 pups on standard food to 18 pups on sucrose. However, TRrGH mice did not attain the reproductive success of normal mice on any diet. These results suggest that TRrGH mice are energetically stressed by enforced channelling of energy into growth. An immense literature addresses infertility due to energy limitation and stress generally. We synthesize these aspects with growth hormone transgenesis to derive an integrated view of neuroendocrine energy regulation relevant to restoring fertility of transgenic GH animals.
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Yang, Jichun, Lihong Chen, Xiaoyan Zhang, Yunfeng Zhou, Dongjuan Zhang, Ming Huo, and Youfei Guan. "PPARs and Female Reproduction: Evidence from Genetically Manipulated Mice." PPAR Research 2008 (2008): 1–8. http://dx.doi.org/10.1155/2008/723243.
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Peroxisome proliferator-activated receptors (PPARs) are ligand-activated nuclear receptors controlling many important physiological processes, including lipid and glucose metabolism, energy homeostasis, inflammation, as well as cell proliferation and differentiation. In the past decade, intensive study of PPARs has shed novel insight into prevention and treatment of dyslipidemia, insulin resistance, and type 2 diabetes. Recently, a large body of research revealed that PPARs are also functionally expressed in reproductive organs and various parts of placenta during pregnancy, which strongly suggests that PPARs might play a critical role in reproduction and development, in addition to their central actions in energy homeostasis. In this review, we summarize recent findings elucidating the role of PPARs in female reproduction, with particular focus on evidence from gene knockout and transgenic animal model study.
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Reese, Jeff, Xuemei Zhao, Wen-Ge Ma, Naoko Brown, Timothy J. Maziasz, and S. K. Dey. "Comparative Analysis of Pharmacologic and/or Genetic Disruption of Cyclooxygenase-1 and Cyclooxygenase-2 Function in Female Reproduction in Mice*." Endocrinology 142, no. 7 (July 1, 2001): 3198–206. http://dx.doi.org/10.1210/endo.142.7.8307.
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Abstract Cyclooxygenase (COX)-derived prostaglandins are critical in female reproduction. Gene targeting studies show that ovulation, fertilization, implantation, and decidualization are defective in COX-2 deficient mice. We used genetic and pharmacologic approaches to perturb COX function and examine the differential and synergistic effects of inhibition of COX-1, COX-2, or of both isoforms on reproductive outcomes during early pregnancy in mice. The results demonstrate that simultaneous inhibition of COX-1 and COX-2 produces more severe effects on early pregnancy events than inhibition of either isoform alone. The effects of pharmacological inhibition of COX-2 on female reproductive functions were less severe than the null mutation of the COX-2 gene. A combined approach showed that COX-2 inhibition in COX-1−/− mice induced complete reproductive failure, suggesting a lack of alternative sources of prostaglandin synthesis. This investigation raises caution regarding the indiscriminate use of COX inhibitors and shows for the first time the distinct and overlapping pathways of the cyclooxygenase systems in female reproduction.
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Harrington, Monica. "Common disinfectants impair reproduction in mice." Lab Animal 43, no. 10 (September 19, 2014): 335. http://dx.doi.org/10.1038/laban.635.
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Yang, Haoxuan, Izhar Hyder Qazi, Bo Pan, Christiana Angel, Shichao Guo, Jingyu Yang, Yan Zhang, et al. "Dietary Selenium Supplementation Ameliorates Female Reproductive Efficiency in Aging Mice." Antioxidants 8, no. 12 (December 11, 2019): 634. http://dx.doi.org/10.3390/antiox8120634.
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Female reproductive (ovarian) aging is distinctively characterized by a markedly reduced reproductive function due to a remarkable decline in quality and quantity of follicles and oocytes. Selenium (Se) has been implicated in playing many important biological roles in male fertility and reproduction; however, its potential roles in female reproduction, particularly in aging subjects, remain poorly elucidated. Therefore, in the current study we used a murine model of female reproductive aging and elucidated how different Se-levels might affect the reproductive efficiency in aging females. Our results showed that at the end of an 8-week dietary trial, whole-blood Se concentration and blood total antioxidant capacity (TAOC) were significantly reduced in Se-deficient (0.08 mg Se/kg; Se-D) mice, whereas both of these biomarkers were significantly higher in inorganic (0.33 mg/kg; ISe-S) and organic (0.33 mg/kg; OSe-S) Se-supplemented groups. Similarly, compared to the Se-D group, Se supplementation significantly ameliorated the maintenance of follicles and reduced the rate of apoptosis in ovaries. Meanwhile, the rate of in vitro-produced embryos resulting from germinal vesicle (GV) oocytes was also significantly improved in Se-supplemented (ISe-S and OSe-S) groups compared to the Se-D mice, in which none of the embryos developed to the hatched blastocyst stage. RT-qPCR results revealed that mRNA expression of Gpx1, Gpx3, Gpx4, Selenof, p21, and Bcl-2 genes in ovaries of aging mice was differentially modulated by dietary Se levels. A considerably higher mRNA expression of Gpx1, Gpx3, Gpx4, and Selenof was observed in Se-supplemented groups compared to the Se-D group. Similarly, mRNA expression of Bcl-2 and p21 was significantly lower in Se-supplemented groups. Immunohistochemical assay also revealed a significantly higher expression of GPX4 in Se-supplemented mice. Our results reasonably indicate that Se deficiency (or marginal levels) can negatively impact the fertility and reproduction in females, particularly those of an advancing age, and that the Se supplementation (inorganic and organic) can substantiate ovarian function and overall reproductive efficiency in aging females.
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Hicks, Kristina L., Elysia Roche, James D. Wilkerson, and Krista E. Lindstrom. "Effects of Maternal Fenbendazole on Litter Size, Survival Rate, and Weaning Weight in C57BL/6J Mice." Journal of the American Association for Laboratory Animal Science 60, no. 6 (November 1, 2021): 630–36. http://dx.doi.org/10.30802/aalas-jaalas-21-000056.
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Fenbendazole is a broad-spectrum benzimidazole commonly used in laboratory animal medicine as an anthelmintic for elimination of pinworms. This drug is generally regarded as safe, with minimal side effects. Some data in rodent species indicate multiple physiologic effects of fenbendazole, including changes in immune parameters and behavior, but no studies to date have evaluated possible effects on reproduction in mice. The purpose of the current study was to determine the effects of several treatment regimens of fenbendazole on reproductive parameters in C57BL/6J mice. Uninfected mice were given fenbendazole-treated feed continuously or every other week until pups were born or weaned. This treatment also was combined with environmental decontamination. No significant differences in litter size, survival rate, or weaning weight were detected between groups. Under the conditions of this study, fenbendazole treatment does not affect reproduction in C57BL/6J mice.
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Roy, Angshumoy, and Martin M. Matzuk. "Deconstructing mammalian reproduction: using knockouts to define fertility pathways." Reproduction 131, no. 2 (February 2006): 207–19. http://dx.doi.org/10.1530/rep.1.00530.
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Reproduction is the sine qua non for the propagation of species and continuation of life. It is a complex biological process that is regulated by multiple factors during the reproductive life of an organism. Over the past decade, the molecular mechanisms regulating reproduction in mammals have been rapidly unraveled by the study of a vast number of mouse gene knockouts with impaired fertility. The use of reverse genetics to generate null mutants in mice through targeted disruption of specific genes has enabled researchers to identify essential regulators of spermatogenesis and oogenesis in vivo and model human disorders affecting reproduction. This review focuses on the merits, utility, and the variations of the knockout technology in studies of reproduction in mammals.
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Hollister, Anne, Patricia Okubara, J. Gary Watson, and Sterling Chaykin. "Reproduction in mice: Liver enlargement in mice during pregnancy and lactation." Life Sciences 40, no. 1 (January 1987): 11–18. http://dx.doi.org/10.1016/0024-3205(87)90246-3.
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Luo, Rongrong, Lei Chen, Xingxing Song, Xin Zhang, Wenhao Xu, Dongyang Han, Jianyu Zuo, et al. "Possible Role of GnIH as a Novel Link between Hyperphagia-Induced Obesity-Related Metabolic Derangements and Hypogonadism in Male Mice." International Journal of Molecular Sciences 23, no. 15 (July 22, 2022): 8066. http://dx.doi.org/10.3390/ijms23158066.
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Gonadotropin-inhibitory hormone (GnIH) is a reproductive inhibitor and an endogenous orexigenic neuropeptide that may be involved in energy homeostasis and reproduction. However, whether GnIH is a molecular signal link of metabolism and the reproductive system, and thus, regulates reproductive activity as a function of the energy state, is still unknown. In the present study, we investigated the involvement of GnIH in glycolipid metabolism and reproduction in vivo, and in the coupling between these two processes in the testis level. Our results showed that chronic intraperitoneal injection of GnIH into male mice not only increased food intake and altered meal microstructure but also significantly elevated body mass due to the increased mass of liver and epididymal white adipose tissue (eWAT), despite the loss of testicular weight. Furthermore, chronic intraperitoneal administration of GnIH to male mice resulted in obesity-related glycolipid metabolic derangements, showing hyperlipidemia, hyperglycemia, glucose intolerance, and insulin resistance through changes in the expression of glucose and lipid metabolism-related genes in the pancreas and eWAT, respectively. Interestingly, the expression of GnIH and GPR147 was markedly increased in the testis of mice under conditions of energy imbalance, such as fasting, acute hypoglycemia, and hyperglycemia. In addition, chronic GnIH injection markedly inhibited glucose and lipid metabolism of mice testis while significantly decreasing testosterone synthesis and sperm quality, inducing hypogonadism. These observations indicated that orexigenic GnIH triggers hyperphagia-induced obesity-related metabolic derangements and hypogonadism in male mice, suggesting that GnIH is an emerging candidate for coupling metabolism and fertility by involvement in obesity and metabolic disorder-induced reproductive dysfunction of the testes.
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Nonomura, M., K. Hoshino, T. Harigaya, H. Hashimoto, and O. Yoshida. "Effects of hyperprolactinaemia on reproduction in male mice." Journal of Endocrinology 107, no. 1 (October 1985): 71–76. http://dx.doi.org/10.1677/joe.0.1070071.
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ABSTRACT Hyperprolactinaemia induced by pituitary isografts in male host mice was confirmed by radioimmunoassay, but plasma testosterone levels determined by radioimmunoassay in these mice showed no changes. Immunoenzyme electron microscopic observations revealed large spherical-shaped immunoreactive prolactin granules in pituitary grafts in male hosts, regardless of the sex of the donor mice, indicating the disappearance of sexual dimorphism in prolactin-producing cells in hyperprolactinaemic mice. In hyperprolactinaemic host mice the male accessory sex glands, particularly the seminal vesicle and the ventral prostate, exhibited considerable proliferation and significant increase in weight. These phenomena do not seem to be mediated by the increased action of testosterone. Such biological effects in host mice were much greater when the donor was female rather than male, and were more noticeable in C57BL mice than in C3H mice. J. Endocr. (1985) 107, 71–76
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Embree-Ku, Michelle, and Kim Boekelheide. "Absence of p53 and FasL Has Sexually Dimorphic Effects on Both Development and Reproduction." Experimental Biology and Medicine 227, no. 7 (July 2002): 545–53. http://dx.doi.org/10.1177/153537020222700720.
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Reproduction and development are highly dependent on apoptosis to balance the proliferation that necessarily occurs during these processes. How the absence of two apoptotic factors in mice would affect reproduction and development was examined. Given previous reports of increased neural tube defects in p53–/– female fetuses, decreased fertility in gld female mice, and altered spermatogenesis in both p53 and gld male mice, the possibility that these phenotypes might be enhanced by the elimination of a second apoptotic factor was investigated. The reproductive vigor and the health of offspring were monitored during the production of the new double-deficient strain (FasL–/–p53–/–) for any changes from the reported phenotypes. Thus, any unusual phenotypes that could lead to new models for studying mechanisms of health and disease would be identified. Double-deficient male offspring appeared healthy and occurred at expected frequencies. Additionally, spermatogenesis and male fertility were unaffected by the gene deficiencies. On the other hand, FasL+/+p53–/– and FasL–/–p53–/– female mice were susceptible to increased malformations and post-natal death. These abnormalities were consistent with previous reports of neural tube defects in p53–/– female mice. Fertility rates were also significantly decreased in p53-/- female mice that lived to be adults, an observation not previously reported. Finally, the absence of both FasL and p53 led to dystocia in pregnant female mice, suggesting that the two genes play complementary roles in parturition. Therefore, although male mouse development and reproduction remained unaffected by p53 and FasL deficiencies, female mouse development was adversely affected by the absence of p53, and no live litters were born to female mice with the combined absence of both FasL and p53. In this report, we suggest a potential mechanism involving corpora luteal regression to explain this defect in parturition in FasL–/–p53–/– female mice.
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Li, Biao, Zhihui Yang, Jingwen Hou, April McCracken, M. Anita Jennings, and Mark Y. J. Ma. "Compromised Reproductive Function in Adult Female Mice Selectively Expressing Mutant ErbB-1 Tyrosine Kinase Receptors in Astroglia." Molecular Endocrinology 17, no. 11 (November 1, 2003): 2365–76. http://dx.doi.org/10.1210/me.2003-0023.
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Abstract The ErbB-1 tyrosine kinase receptor plays critical roles in regulating physiological functions. This receptor-mediated signaling in astroglia has been implicated in controlling female sexual development via activating neurons that release LH-releasing hormone (LHRH), the neuropeptide required for the secretion of LH. It remains unknown whether astroglial ErbB-1 receptors are necessary for maintaining normal adult reproductive function. Here we provide genetic evidence that astroglia-specific and time-controlled disruption of ErbB-1 receptor signaling by expressing mutant ErbB-1 receptors leads to compromised reproduction due to alteration in LHRH neuron-controlled secretion of LH in adult female mice. Therefore, astroglial ErbB-1 receptors are required for controlling LHRH neuronal function and thus maintaining adult reproduction, suggesting that compromised astroglial ErbB-1 signaling may also contribute to reproductive abnormalities in aging females.
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Jackson, C., and R. T. F. Bernard. "Effects of supplementary food on the winter inhibition of reproduction in male and female four-striped field mice (Rhabdomys pumilio)." Reproduction, Fertility and Development 17, no. 4 (2005): 393. http://dx.doi.org/10.1071/rd04134.
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The effects of winter food supplementation on reproduction in the seasonally breeding four-striped field mouse Rhabdomys pumilio were investigated at Mountain Zebra National Park in the Eastern Cape Province of South Africa. On both control and supplemented grids, reproductive activity in females was inhibited; no pregnant females were collected and juveniles were only present in the first winter month. The provision of additional food resulted in an increase in body mass and mass of the male and female reproductive organs. However, all males, from both grids, were spermatogenically active. Ovarian activity was not stimulated by the provision of additional food, but the development of the uterus was and the endometrium was thicker and more vascularised in mice from the supplemented grid than from the control grid. We conclude that seasonal reproduction in R. pumilio is controlled by the females, in which reproductive activity is inhibited in winter. However, the provision of supplementary food was not sufficient to override the reproductive inhibition.
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Nohara, Kazunari, Suhuan Liu, Matthew S. Meyers, Aurélie Waget, Mathieu Ferron, Gérard Karsenty, Rémy Burcelin, and Franck Mauvais-Jarvis. "Developmental androgen excess disrupts reproduction and energy homeostasis in adult male mice." Journal of Endocrinology 219, no. 3 (October 1, 2013): 259–68. http://dx.doi.org/10.1530/joe-13-0230.
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Polycystic ovary syndrome is a common endocrine disorder in females of reproductive age and is believed to have a developmental origin in which gestational androgenization programs reproductive and metabolic abnormalities in offspring. During gestation, both male and female fetuses are exposed to potential androgen excess. In this study, we determined the consequences of developmental androgenization in male mice exposed to neonatal testosterone (NTM). Adult NTM displayed hypogonadotropic hypogonadism with decreased serum testosterone and gonadotropin concentrations. Hypothalamic KiSS1 neurons are believed to be critical to the onset of puberty and are the target of leptin. Adult NTM exhibited lower hypothalamicKiss1expression and a failure of leptin to upregulateKiss1expression. NTM displayed an early reduction in lean mass, decreased locomotor activity, and decreased energy expenditure. They displayed a delayed increase in subcutaneous white adipose tissue amounts. Thus, excessive neonatal androgenization disrupts reproduction and energy homeostasis and predisposes to hypogonadism and obesity in adult male mice.
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MCBURNIE, M., J. BLAIRWEST, D. DENTON, and R. WEISINGER. "Sodium Intake and Reproduction in BALB/C Mice." Physiology & Behavior 66, no. 5 (July 1999): 873–79. http://dx.doi.org/10.1016/s0031-9384(99)00034-7.
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Höglund, N. J. "Effects of Ethyl Urethane on Reproduction in Mice." Acta Pharmacologica et Toxicologica 8, no. 1 (March 13, 2009): 82–84. http://dx.doi.org/10.1111/j.1600-0773.1952.tb02887.x.
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Pye, T. "Reproductive biology of the feral house mouse (Mus musculus) on subantarctic Macquarie Island." Wildlife Research 20, no. 6 (1993): 745. http://dx.doi.org/10.1071/wr9930745.
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Reproduction of the feral house mouse (Mus musculus) was studied on subantarctic Macquarie Island and found to be seasonal. Females begin oestrus-cycling in early spring, following a minimum 3-month winter anoestrous period. By late spring all mature females are in breeding condition. Breeding is continuous through spring, summer and into autumn. Postimplantation loss occurs throughout the breeding season. Late autumn pregnancies may fail. Average litter size is 6-7 but litters as large as 10 have been found. Young born in the latter half of the breeding season attain sexual maturity at a later stage than those born in the early-spring-summer period and do not come into breeding condition until the following spring. Males show a slight cyclical change in testes weight, increasing from a winter minimum to a summer maximum, but are potentially capable of breeding throughout the year. Reproductive seasonality of the female determines breeding behaviour in this isolated subantarctic population of feral house mice. Seasonal reproduction is not well correlated with mean monthly ambient temperature, which varies by only 3O degrees C over the year. Food availability appears constant throughout the year with little interspecific competition for food or predation on the mice. Reproduction is suppressed over the short-day winter months. The possible interaction of photoperiod with other environmental and physiological variables in determining reproductive seasonality requires further research.
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Kiyosu, Chiyo, Takehito Tsuji, Kaoru Yamada, Shimpei Kajita, and Tetsuo Kunieda. "NPPC/NPR2 signaling is essential for oocyte meiotic arrest and cumulus oophorus formation during follicular development in the mouse ovary." REPRODUCTION 144, no. 2 (August 2012): 187–93. http://dx.doi.org/10.1530/rep-12-0050.
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Natriuretic peptide type C (NPPC) and its high affinity receptor, natriuretic peptide receptor 2 (NPR2), have been assumed to be involved in female reproduction and have recently been shown to play an essential role in maintaining meiotic arrest of oocytes. However, the overall role of NPPC/NPR2 signaling in female reproduction and ovarian function is still less clear. Here we report the defects observed in oocytes and follicles of mice homozygous for Nppclbab or Npr2cn, mutant alleles of Nppc or Npr2 respectively to clarify the exact consequences of lack of NPPC/NPR2 signaling in female reproductive systems. We found that: i) Npr2cn/Npr2cn female mice ovulated a comparable number of oocytes as normal mice but never produced a litter; ii) all ovulated oocytes of Npr2cn/Npr2cn and Nppclbab/Nppclbab mice exhibited abnormalities, such as fragmented or degenerated ooplasm and never developed to the two-cell stage after fertilization; iii) histological examination of the ovaries of Npr2cn/Npr2cn and Nppclbab/Nppclbab mice showed that oocytes in antral follicles prematurely resumed meiosis and that immediately before ovulation, oocytes showed disorganized chromosomes or fragmented ooplasm; and iv) ovulated oocytes and oocytes in the periovulatory follicles of the mutant mice were devoid of cumulus cells. These findings demonstrate that NPPC/NPR2 signaling is essential for oocyte meiotic arrest and cumulus oophorus formation, which affects female fertility through the production of oocytes with developmental capacity.
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Kennaway, D. J., A. Voultsios, and M. J. Boden. "241.Reproductive performance in Clock mutant mice." Reproduction, Fertility and Development 16, no. 9 (2004): 241. http://dx.doi.org/10.1071/srb04abs241.
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The relationship between circadian rhythmicity and rodent reproductive cyclicity is well established, but the impact of disrupted clock gene function on reproduction has not been investigated. This study evaluated the reproductive performance of melatonin deficient and proficient mice carrying a mutation in the core circadian gene, Clock. In natural matings, melatonin deficient Clock mutant mice took 2 to 3 days longer to mate and to subsequently deliver pups than their control line. The melatonin proficient mutants (Clock-MEL) had a smaller, but still significant delay (P < 0.05). The Clock mutation resulted in smaller median litter sizes compared to the control lines (7 v. 8 pups, P < 0.05) while melatonin proficiency reversed this difference. Survival to weaning was 84% and 80% for the melatonin deficient and proficient Clock mutant lines respectively, compared to 94 to 96% for their control lines. When immature mice were subjected to a standard PMSG/HCG superovulation protocol, Clock-MEL mice had lowered fertility and significantly fewer ovulations than their control line although embryo development appeared to be only slightly affected (Table 1, see PDF file).
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Zhang, JinFu, YaPing Gui, Tao Yuan, CuiDong Bian, and LiHe Guo. "Expression of GAT1 in Male Reproductive System and its Effects on Reproduction in Mice." Systems Biology in Reproductive Medicine 55, no. 5-6 (January 2009): 175–80. http://dx.doi.org/10.3109/19396360903030500.
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Ratajczak, Christine K., Katie L. Boehle, and Louis J. Muglia. "Impaired Steroidogenesis and Implantation Failure in Bmal1−/− Mice." Endocrinology 150, no. 4 (December 4, 2008): 1879–85. http://dx.doi.org/10.1210/en.2008-1021.
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Evidence in humans and rodents suggests that normal circadian rhythmicity is important for supporting reproductive function. A molecular clock underlies circadian rhythmicity. Impaired fertility is observed in some genetically altered mice with deficiencies in genes of the molecular clock, suggesting a critical role for these genes in reproduction. Here we systematically characterize the reproductive phenotype of females deficient in the clock gene Bmal1. Bmal1−/− females are infertile. They exhibit progression through the estrous cycle, although these cycles are prolonged. Normal follicular development occurs in Bmal1−/− females, and healthy embryos of the expected developmental stage are found in the reproductive tract of Bmal1−/− females 3.5 d after mating to wild-type males. However, serum progesterone levels are significantly lower in Bmal1−/−vs. Bmal1+/± females on d 3.5 of gestation. Low progesterone levels in Bmal1−/− females are accompanied by decreased expression of steroidogenic acute regulatory protein in corpora lutea of Bmal1−/−vs. Bmal1+/± females. Whereas implantation of embryos is not observed in untreated or vehicle-treated Bmal1−/− females, exogenous administration of progesterone to Bmal1−/− females is able to reinstitute implantation. These data suggest that implantation failure due to impaired steroidogenesis causes infertility of Bmal1−/− females.
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Gouat, Patrick, Christophe Féron, and Simone Demouron. "Seasonal reproduction and delayed sexual maturity in mound-building mice Mus spicilegus." Reproduction, Fertility and Development 15, no. 3 (2003): 187. http://dx.doi.org/10.1071/rd02105.
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In the mound-building mouse, Mus spicilegus, which is found from Central to Eastern Europe, reproduction is seasonal and limited to spring and summer. In autumn, the mice build voluminous mounds composed of vegetable matter covered with earth, where juvenile animals (autumnal individuals) over-winter in groups without reproducing. Autumnal animals delay reproduction until the next spring when they are 6 months old. The influence and interactions of environmental (short light period and cold temperature (C conditions) compared with long light period and temperate temperature (T conditions)) and social factors (lack of odours from breeding adults (NB conditions) compared with presence of odours from breeding adults (B conditions)) on reproduction and sexual maturation were studied. Forty groups of three autumnal individuals (two males and a female or two females and a male) were placed in four experimental conditions (CB, CNB, TB and TNB), corresponding to interactions between environmental and social factors (n = 10 groups for each condition). Of the 40 groups only one initiated reproduction during the 18 weeks of cohabitation. Subsequently, animals were separated and isolated for 1 month and then paired with unfamiliar partners. Reproduction was monitored for an additional month, and 24 out of 39 females reproduced. In addition, of eight reproducing pairs placed in C conditions and 10 reproducing pairs maintained in T conditions, all but one pair continued reproduction. It was concluded that the delay in reproduction observed in autumnal individuals was the result of the social effects of living in groups as opposed to the environmental conditions of winter.
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Kinnear, H. M., E. S. Constance, A. David, E. E. Marsh, V. Padmanabhan, A. Shikanov, and M. B. Moravek. "A mouse model to investigate the impact of testosterone therapy on reproduction in transgender men." Human Reproduction 34, no. 10 (October 2019): 2009–17. http://dx.doi.org/10.1093/humrep/dez177.
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Abstract STUDY QUESTION Can mice serve as a translational model to investigate the reproductive effects of testosterone (T) therapy commonly used by transgender men? SUMMARY ANSWER T enanthate subcutaneous injections at 0.45 mg twice weekly can be used in the postpubertal C57BL/6N female mouse to investigate the reproductive effects of T therapy given to transgender men. WHAT IS KNOWN ALREADY Most models of T treatment in female mice involve prenatal or prepubertal administration, which are not applicable to transgender men who often begin T therapy after puberty. Studies that have looked at the impact of postpubertal T treatment in female mice have generally not investigated reproductive outcomes. STUDY DESIGN, SIZE, DURATION A total of 20 C57BL/6N female mice were used for this study. Study groups (n = 5 mice per group) included sesame oil vehicle controls and three doses of T enanthate (0.225, 0.45 and 0.90 mg). Mice were injected subcutaneously twice weekly for 6 weeks. PARTICIPANTS/MATERIALS, SETTING, METHODS Daily vaginal cytology was performed prior to initiation of treatment to confirm that all mice were cycling. At 8–9 weeks of age, therapy with subcutaneous T enanthate (0.225, 0.45 or 0.90 mg) or the vehicle control was begun. T therapy continued for 6 weeks, at which point mice were sacrificed and compared to control mice sacrificed during diestrus/metestrus. Data collected included daily vaginal cytology, weekly and terminal reproductive hormone levels, terminal body/organ weights/measurements, ovarian follicular distribution/morphology and corpora lutea counts. MAIN RESULTS AND THE ROLE OF CHANCE Of the mice treated with 0.90 mg T enanthate, two of five mice experienced vaginal prolapse, so this group was excluded from further analysis. T enanthate administration twice weekly at 0.225 or 0.45 mg resulted in cessation of cyclicity and persistent diestrus. One of five mice at the 0.225-mg dose resumed cycling after 2.5 weeks of T therapy. As compared to controls, T-treated mice had sustained elevated T levels and luteinizing hormone (LH) suppression in the terminal blood sample. T-treated mice demonstrated increases in clitoral area and atretic cyst-like late antral follicles (0.45 mg only) as compared to controls. No reduction in primordial, primary, secondary or total antral follicle counts was detected in T-treated mice as compared to controls, and T-treated mice demonstrated an absence of corpora lutea. LIMITATIONS, REASONS FOR CAUTION Mouse models can provide us with relevant key findings for further exploration but may not perfectly mirror human reproductive physiology. WIDER IMPLICATIONS OF THE FINDINGS To our knowledge, this report describes the first mouse model mimicking T therapy given to transgender men that facilitates analysis of reproductive changes. This model allows for future studies comparing duration and reversibility of T-induced changes, on the reproductive and other systems. It supports a role for T therapy in suppressing the hypothalamic–pituitary–gonadal axis in adult female mice as evidenced by LH suppression, persistent diestrus and absence of corpora lutea. The increase in atretic cyst-like late antral follicles aligns with the increased prevalence of polycystic ovary morphology seen in case series of transgender men treated with T therapy. The results also suggest that T therapy does not deplete the ovarian reserve. STUDY FUNDING/COMPETING INTEREST(S) This work was supported by the American Society for Reproductive Medicine/Society of Reproductive Endocrinology and Infertility Grant and NIH R01-HD098233 to M.B.M. and University of Michigan Office of Research funding (U058227). H.M.K. was supported by the Career Training in Reproductive Biology and Medical Scientist Training Program T32 NIH Training Grants (T32-HD079342, T32-GM07863) as well as the Cellular and Molecular Biology Program. The University of Virginia Center for Research in Reproduction Ligand Assay and Analysis Core is supported by the Eunice Kennedy Shriver NICHD/NIH (NCTRI) Grant P50-HD28934. E.E.M. consults for Allergan. No other authors have competing interests.
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Rocha, Juliana S., Michael S. Bonkowski, Luiz R. França, and Andrzej Bartke. "Mild Calorie Restriction Does Not Affect Testosterone Levels and Testicular Gene Expression in Mutant Mice." Experimental Biology and Medicine 232, no. 8 (September 2007): 1050–63. http://dx.doi.org/10.3181/0703-rm-52.
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The hypothalamic-pituitary-gonadal (HPG) axis and the somatotropic axis are influenced by nutritional factors. Calorie restriction (CR) extends lifespan but suppresses both the HPG and the somatotropic axes. Since most CR studies use a fairly severe (40%–60%) reduction of calorie intake, we hypothesized that a milder CR (20%) might not be deleterious to reproduction in male mice. To test this hypothesis, we evaluated the effects of 20% CR on testicular testosterone content and on testicular expression of genes that are relevant to testicular function and reproductive competence, including insulin-like growth factor-I, cytochrome P450 aromatase (Cyp19a1), androgen receptor, luteinizing hormone receptor, follicle-stimulating hormone receptor, cytochrome P450c17 and 3-β-hydroxysteroid dehydrogenase/isomerase. To relate CR effects to the activity of the somatotropic axis, we have used growth hormone–resistant GHR knockout mice as well as transgenic mice overexpressing GH. Mild CR did not affect testosterone levels in testis homogenates and had little effect on expression of the examined genes in the reproductive organs. Altered activity of the GH/insulin-like growth factor–1 axis had a major impact on the parameters analyzed. The results also suggest that expression of several key genes involved in the control of testicular function is preserved under conditions of mild CR and encourage speculation that mild regimens of CR can produce longevity benefits without impairing reproduction.
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Huang, Yinqiong, Junping Wen, and Gang Chen. "Role and Mechanism of Chronic Restraint Stress in Regulating Energy Metabolism and Reproductive Function Through Hypothalamic Kisspeptin Neurons." Journal of the Endocrine Society 5, Supplement_1 (May 1, 2021): A551—A552. http://dx.doi.org/10.1210/jendso/bvab048.1124.
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Abstract Objectives: The purpose of this study was to investigate whether stress affected energy metabolism and reproductive function through the glucocorticoid receptor (GR) on Kisspeptin neurons in the hypothalamus. Methods: 1. The first part of this study focused on the effects of chronic restraint stress on energy metabolism and reproductive function in mice. 2. The second part of this study focused on the effects of chronic restraint stress on the expression of serum cortisol and prolactin and the expression of GR and Kiss1 genes in the hypothalamus.3. Based on the above research, we constructed Kisspeptin specific glucocorticoid receptor knock out (KGRKO) mice. The mice were subjected to restraint stress intervention, the body weight of the mice was monitored every day, and the vaginal smear was performed on the female mice to observe the estrous cycle. After 28 days of restraint stress, serum was collected to detect serum sex hormone levels, including LH, FSH and estrogen levels in female mice and testosterone level in male mice by ELISA. Results: 1.The body weight and energy intake of the restraint stress group were lower than those of the control. 2.After restraint stress, the female mice showed irregular estrous cycle. LH and FSH levels in the stress group were significantly decreased compared with the control group.3. After restraint stress, the levels of serum cortisol and prolactin in male and female mice were significantly higher than the control group, and the hypothalamus Kiss1 gene mRNA expression and Kisspeptin protein expression were significantly decreased.4. In female mice, compared with GRflox/flox/Kiss1Cre-control mice, the nadir serum cortisol increased significantly in the morning in GRflox/flox/Kiss1Cre+ KGRKO mice, however, there was no significant difference in the serum peak cortisol in the afternoon. Compared with the control group, the restraint stress group and the KGRKO + restraint stress group had a significant weight loss compared with the KGRKO group. Compared with the restraint stress group, the KGRKO+restraint stress group had a reduced weight loss, suggesting that restraint stress might partially affect the energy metabolism through GR on Kisspeptin neurons. Conclusions: Chronic restraint stress induced weight loss in mice and reversed body weight gain induced by high-fat diet. Chronic restraint stress played a negative role in regulating reproductive function. The effects of chronic restraint stress on energy metabolism and reproduction were partially mediated by GR on Kisspeptin neurons in the hypothalamus. This study provided a central mechanism for chronic restraint stress in affecting energy metabolism and reproductive function, and was of great significance in revealing the relationship between the HPA axis with energy metabolism and reproduction.
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Shimshek, Derya R., Thorsten Bus, Valery Grinevich, Frank N. Single, Volker Mack, Rolf Sprengel, Daniel J. Spergel, and Peter H. Seeburg. "Impaired Reproductive Behavior by Lack of GluR-B Containing AMPA Receptors But Not of NMDA Receptors in Hypothalamic and Septal Neurons." Molecular Endocrinology 20, no. 1 (January 1, 2006): 219–31. http://dx.doi.org/10.1210/me.2005-0262.
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Abstract The roles of ionotropic glutamate receptors in mammalian reproduction are unknown. We therefore generated mice lacking a major subtype of (S)-α-amino-3-hydroxy-5-methyl-isoxazolepropionic acid (AMPA) receptors or all N-methyl-d-aspartate (NMDA) receptors in GnRH neurons and other mainly limbic system neurons, primarily in hypothalamic and septal areas. Male mice without NMDA receptors in these neurons were not impaired in breeding and exhibited similar GnRH secretion as control littermates. However, male mice lacking GluR-B containing AMPA receptors in these neurons were poor breeders and severely impaired in reproductive behaviors such as aggression and mounting. Testis and sperm morphology, testis weight, and serum testosterone levels, as well as GnRH secretion, were unchanged. Contact with female cage bedding failed to elicit male sexual behavior in these mice, unlike in control male littermates. Their female counterparts had unchanged ovarian morphology, had bred successfully, and had normal litter sizes but exhibited pronounced impairments in maternal behaviors such as pup retrieval and maternal aggression. Our results suggest that NMDA receptors and GluR-B containing AMPA receptors are not essential for fertility, but that GluR-B containing AMPA receptors are essential for male and female reproduction-related behaviors, perhaps by mediating responses to pheromones or odorants.
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Garratt, Michael, Heather Try, Kristina O. Smiley, David R. Grattan, and Robert C. Brooks. "Mating in the absence of fertilization promotes a growth-reproduction versus lifespan trade-off in female mice." Proceedings of the National Academy of Sciences 117, no. 27 (June 22, 2020): 15748–54. http://dx.doi.org/10.1073/pnas.2003159117.
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Trade-offs between growth, reproduction, and lifespan constrain animal life histories, leading to evolutionary diversification of life history cycles in different environments. In female mammals, gestation and lactation are expected to impose the major costs of reproduction, driving reproductive trade-offs, although mating also requires interactions with males that could themselves influence life history. Here we show that a male’s presence by itself leads to lifelong alterations in life history in female mice. Housing C57BL/6J female mice with sterilized males early in life led to an increase in body weight, an effect that persisted across life even when females were later allowed to produce pups. We found that those females previously housed with sterile males also showed enhanced late-life offspring production when allowed to reproduce, indicating that earlier mating can influence subsequent fecundity. This effect was the opposite to that seen in females previously housed with intact males, which showed the expected trade-off between early-life and late-life reproduction. However, housing with a sterile male early in life came at a cost to lifespan, which was observed in the absence of females ever undergoing fertilization. Endocrinologically, mating also permanently reduced the concentration of circulating prolactin, a pituitary hormone influencing maternal care. Changes in hormone axes that influence reproduction could therefore help alter life history allocation in response to opposite-sex stimuli. Our results demonstrate that mating itself can increase growth and subsequent fecundity in mammals, and that responses to sexual stimuli could account for some lifespan trade-offs normally attributed to pregnancy and lactation.
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Antolová, D., and K. Reiterová. "The course of Echinococcus multilocularis infection and pregnancy in mice model." Helminthologia 48, no. 4 (December 1, 2011): 251–55. http://dx.doi.org/10.2478/s11687-011-0035-1.
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AbstractParasitic infection during pregnancy can affect the course of pregnancy, complicate the foeto-maternal relationship and increase abortion rate. The work was aimed to study the course of E. multilocularis secondary infection and reproductive parameters in infected mice. The Balb/c mice were bred in the exponential phase of the metacestode growth, after infection with two different doses (0.5 ml or 1.25 ml) of metacestode material. In comparison to uninfected control group, the effect of infection on reproductive parameters (natality, size of litters) and the course of disease during pregnancy and after the delivery were monitored. The weight of E. multilocularis larval stages was higher in both fertilised groups in comparison to unfertilised control. The number of deliveries and litter counts were similar in both, infected and uninfected mice. Present study confirmed only minor impact of alveolar echinococcosis on the reproduction of rodents, intermediate hosts of parasite.
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Martin, J. Ryan, Sarah B. Lieber, James McGrath, Marya Shanabrough, Tamas L. Horvath, and Hugh S. Taylor. "Maternal Ghrelin Deficiency Compromises Reproduction in Female Progeny through Altered Uterine Developmental Programming." Endocrinology 152, no. 5 (February 15, 2011): 2060–66. http://dx.doi.org/10.1210/en.2010-1485.
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Ghrelin has a well-known role in the regulation of appetite, satiety, energy metabolism, and reproduction; however ghrelin has not been implicated in reproductive tract development. We examined the effect of ghrelin deficiency on the developmental programming of female fertility. We observed that female wild-type mice born of ghrelin heterozygote dams (i.e. exposed in utero to ghrelin deficiency) had diminished fertility and produced smaller litters. We demonstrate that exposure to in utero ghrelin deficiency led to altered developmental programming of the reproductive tract. The number of ovarian follicles, corpora lutea, and embryos produced were identical in both exposed and unexposed mice. However wild-type embryos transferred to uteri of mice exposed to in utero ghrelin deficiency had a 60% reduction in the rate of embryo implantation compared with those transferred to wild-type unexposed uteri. We identified significant alterations in the uterine expression of four genes critical for implantation and a defect in uterine endometrial proliferation. Taken together, these results demonstrate that the mechanism of subfertility was abnormal endometrial function. In utero exposure to decreased levels of ghrelin led to defects in developmental programming of the uterus and subsequent subfertility in wild-type offspring.
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Klenke, Ulrike, Carol Taylor-Burds, and Susan Wray. "Metabolic Influences on Reproduction: Adiponectin Attenuates GnRH Neuronal Activity in Female Mice." Endocrinology 155, no. 5 (May 1, 2014): 1851–63. http://dx.doi.org/10.1210/en.2013-1677.
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Metabolic dysfunctions are often linked to reproductive abnormalities. Adiponectin (ADP), a peripheral hormone secreted by white adipose tissue, is important in energy homeostasis and appetite regulation. GnRH neurons are integral components of the reproductive axis, controlling synthesis, and release of gonadotropins. This report examined whether ADP can directly act on GnRH neurons. Double-label immunofluorescence on brain sections from adult female revealed that a subpopulation of GnRH neurons express ADP receptor (AdipoR)2. GnRH/AdipoR2+ cells were distributed throughout the forebrain. To determine the influence of ADP on GnRH neuronal activity and the signal transduction pathway of AdipoR2, GnRH neurons maintained in explants were assayed using whole-cell patch clamping and calcium imaging. This mouse model system circumvents the dispersed distribution of GnRH neurons within the forebrain, making analysis of large numbers of GnRH cells possible. Single-cell PCR analysis and immunocytochemistry confirmed the presence of AdipoR2 in GnRH neurons in explants. Functional analysis revealed 20% of the total GnRH population responded to ADP, exhibiting hyperpolarization or decreased calcium oscillations. Perturbation studies revealed that ADP activates AMP kinase via the protein kinase Cζ/liver kinase B1 pathway. The modulation of GnRH neuronal activity by ADP demonstrated in this report directly links energy balance to neurons controlling reproduction.
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Ivanova, Margarita, Klaudia M. Dobrzycka, Shiming Jiang, Kai Michaelis, Rene Meyer, Kaiyan Kang, Brian Adkins, et al. "Scaffold Attachment Factor B1 Functions in Development, Growth, and Reproduction." Molecular and Cellular Biology 25, no. 8 (April 15, 2005): 2995–3006. http://dx.doi.org/10.1128/mcb.25.8.2995-3006.2005.
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ABSTRACT Scaffold attachment factor B1 (SAFB1) is a multifunctional protein that can bind both DNA and RNA and is involved in RNA processing and stress response. In addition, SAFB1 contains a transcriptional repression domain and can bind certain hormone receptors and repress their activity. To assess the role of SAFB1 in vivo, we generated SAFB1 mutant mice through targeted deletion in embryonic stem cells. While viable homozygous mutant (SAFB1−/−) mice were obtained, genotypic distribution indicated that homozygous deficiency resulted in both prenatal and neonatal lethality. Mice lacking SAFB1 exhibited dwarfism, as a result of in utero growth retardation, and had low serum insulin-like growth factor 1 (IGF1) levels. In agreement with the previous characterization of SAFB1 as a corepressor for hormone receptors, we found that SAFB1−/− mice displayed dramatic defects in the development and function of the reproductive system. Male SAFB1 null mice were infertile, apparently because of low circulating levels of testosterone. SAFB1−/− testes were small and showed progressive degeneration of the germinal epithelium, increased apoptosis of germ cells, and Leydig cell hyperplasia. SAFB−/− female mice were subfertile and showed progressive infertility, in part because of defects in oviductal transport and reduced numbers of follicles. Immortalized SAFB1−/− mouse embryonic fibroblasts showed cell-intrinsic defects including increased transcriptional estrogen receptor α activity and enhanced responsiveness to IGF1. Together, these in vivo findings establish a critical role for SAFB1 in development, growth regulation, and reproduction.
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Polotsky, Alex, and Jasmine Aly. "Paternal Diet and Obesity: Effects on Reproduction." Seminars in Reproductive Medicine 35, no. 04 (July 2017): 313–17. http://dx.doi.org/10.1055/s-0037-1602593.
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AbstractAlthough most research has focused on maternal obesity, there is growing data to indicate that obesity in the father can affect reproduction. Supporting data come from both mouse and human studies. Murine studies found that obese male mice exhibited decreased motility and reduced hyperactivated progression versus lean mice. Obese mice also exhibited sperm with increased levels of intracellular and mitochondrial levels of reactive oxygen species, increased sperm damage, and lower levels of capacitation, which has been shown to be associated with poor fertilization rates following in vitro fertilization, defective preimplantation embryonic development, and high rates of miscarriage and morbidity in the offspring. Furthermore, diet-induced paternal obesity was found to initiate intergenerational transmission of obesity and insulin resistance in two generations of murine offspring. Meta-analysis from human studies found obese males were more likely to demonstrate sperm DNA fragmentation, infertility, decreased live birth per cycle of assisted reproduction technology, and increased absolute risk of pregnancy nonviability, with no consistent effect on conventional semen parameters. There is a need for future studies to expound on the mechanisms of sperm DNA damage and the impact of weight loss in reversing this damage.
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Bachelot, Anne, and Nadine Binart. "Reproductive role of prolactin." Reproduction 133, no. 2 (February 2007): 361–69. http://dx.doi.org/10.1530/rep-06-0299.
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The biological actions of prolactin (PRL), a polypeptide hormone, are mostly related to lactation and reproduction. These actions have been clarified by studies of PRL and PRL-deficient receptor mice, which have a clear phenotype of reproductive failure at multiple sites. This review aims to summarize current knowledge about PRL and its receptor, role in reproductive axis and presents information of hyperprolactinemia in reproductive medicine. Our understanding of the physiology and transduction pathway of PRL has largely increased in the past 20 years with the cloning of PRL and its receptor gene.
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TOMIC, D., M. FRECH, J. BABUS, D. SYMONDS, P. FURTH, R. KOOS, and J. FLAWS. "Effects of ERα overexpression on female reproduction in mice." Reproductive Toxicology 23, no. 3 (April 2007): 317–25. http://dx.doi.org/10.1016/j.reprotox.2006.08.004.
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Calle, J., J. Olarte, R. Pinzon, L. F. Ospina, M. C. Mendoza, and M. J. Orozco. "Alterations in the reproduction of mice induced by rapanone." Journal of Ethnopharmacology 71, no. 3 (August 2000): 521–25. http://dx.doi.org/10.1016/s0378-8741(99)00214-7.
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Ishiniwa, Hiroko, Mizuki Sakai, Shimon Tohma, Hidenori Matsuki, Yukio Takahashi, Hideo Kajiwara, and Tsuneo Sekijima. "Dioxin pollution disrupts reproduction in male Japanese field mice." Ecotoxicology 22, no. 9 (September 13, 2013): 1335–47. http://dx.doi.org/10.1007/s10646-013-1120-7.
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Nagai, J., G. Davis, K. Nonaka, and H. Sasada. "Growth and reproduction of mice developed from bisected embryos." Theriogenology 32, no. 3 (September 1989): 475–83. http://dx.doi.org/10.1016/0093-691x(89)90014-9.
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Rocha, Joao L., Eugene J. Eisen, Frank Siewerdt, L. Dale Van Vleck, and Daniel Pomp. "A large-sample QTL study in mice: III. Reproduction." Mammalian Genome 15, no. 11 (November 2004): 878–86. http://dx.doi.org/10.1007/s00335-004-2364-6.
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Ohtsuka, Satoshi, Satoshi Takaki, Masanori Iseki, Kanta Miyoshi, Naomi Nakagata, Yuki Kataoka, Nobuaki Yoshida, Kiyoshi Takatsu, and Akihiko Yoshimura. "SH2-B Is Required for Both Male and Female Reproduction." Molecular and Cellular Biology 22, no. 9 (May 1, 2002): 3066–77. http://dx.doi.org/10.1128/mcb.22.9.3066-3077.2002.
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ABSTRACT Many growth factors and hormones modulate the reproductive status in mammals. Among these, insulin and insulin-like growth factor I (IGF-I) regulate the development of gonadal tissues. SH2-B has been shown to interact with insulin and IGF-I receptors, although the role of SH2-B in these signals has not been clarified. To investigate the role of SH2-B, we generated mice with a targeted disruption of the SH2-B gene. Both male and female SH2-B−/− mice showed slight retardation in growth and impaired fertility. Female knockout mice possess small, anovulatory ovaries with reduced numbers of follicles and male SH2-B−/− mice have small testes with a reduced number of sperm. SH2-B−/− cumulus cells do not respond to either follicle-stimulating hormone or IGF-I. These data suggest that SH2-B plays a critical role in the IGF-I-mediated reproductive pathway in mice.
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Boden, M. J., and D. J. Kennaway. "297. Reproduction in the arrhythmic Bmal1 knockout mouse." Reproduction, Fertility and Development 17, no. 9 (2005): 126. http://dx.doi.org/10.1071/srb05abs297.
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There is strong epidemiological evidence indicating that disruption of the endogenous circadian rhythms can cause a range of health problems ranging from metabolic and cardiovascular disorders to reproductive failure. Circadian rhythmicity is generated by a suite of genes called ‘clock genes’ that are cyclically expressed in the brain and peripheral tissues. The CLOCK and BMAL1 transcription factors regulate the expression of many genes involved in cell growth, angiogenesis and development. The Bmal1 knockout mouse provides an interesting model to analyse the impact of arrhythmicity on reproductive physiology. Female Bmal1–/– mice show a delay in the onset of puberty (WT = 32.7 d, KO = 38.6 d, n = 8–16). Female Bmal1–/– mice reproductive tissues are significantly smaller than in WT mice (Ovaries –40%, Oviduct –25%, Uterus –60%, n = 10). Female Bmal1–/– mice have essentially normal estrus cycles (cycle length WT = 4.2 d, KO = 4.8 d, n = 8) and are able to ovulate and mate but are unable to establish viable pregnancies. They are as responsive to a standard superovulation protocol as their wild type littermates (ovulated oocytes WT = 23.8, KO=22.8, n = 7–10), suggesting the ovaries are developmentally competent. These results suggest disruption of circadian rhythmicity in the mouse affects fertility at multiple sites. Further investigation into the importance of rhythmicity, particularly post ovulation and post fertilisation is required.
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Heideman, Paul D., Julian T. Pittman, Kristin A. Schubert, Christen M. R. Dubois, Jennifer Bowles, Sean M. Lowe, and Matthew R. Price. "Variation in levels of luteinizing hormone and reproductive photoresponsiveness in a population of white-footed mice (Peromyscus leucopus)." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 298, no. 6 (June 2010): R1543—R1548. http://dx.doi.org/10.1152/ajpregu.00686.2009.
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Natural genetic variation in reproduction and life history strategies is a manifestation of variation in underlying regulatory neuronal and endocrine systems. A test of the hypothesis that genetic variation in luteinizing hormone (LH) level could be related to a life history trait, seasonal reproduction, was conducted on artificial selection lines from a wild-source population of white-footed mice ( Peromyscus leucopus ). Variation exists in the degree of suppression of reproduction by winter short-day photoperiods (SD) in wild-source individuals and in the laboratory population. In this population, most individuals from a photoperiod-responsive (R) artificial selection line are strongly suppressed reproductively in SD, while most individuals from a photoperiod-nonresponsive (NR) artificial selection line are only weakly reproductively suppressed in SD. We assayed levels of LH to test for genetic variation between lines that could contribute to variation in reproductive status in SD. Females from both lines were raised in long-day photoperiods (LD) or SD, ovariectomized under isoflurane anesthesia, and given estradiol implants. Levels of LH were significantly higher in the NR line than in the R line, indicating genetic variation for levels of LH. Levels of LH were higher in LD than in SD, indicating that levels of LH were sensitive to photoperiod treatment even with a controlled level of estradiol negative feedback. The results indicate that there is genetic variation in levels of LH that could be functionally important both in the laboratory in SD and in the wild population in winter. Thus genetic variation in levels of LH is a plausible causal factor determining winter reproductive phenotype in the wild population.
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McKenna, Jarrod, Sally Catt, Mulyoto Pangestu, and Peter Temple-Smith. "Successful sperm cryopreservation in Egyptian spiny mice Acomys cahirinus." Reproduction, Fertility and Development 32, no. 16 (2020): 1293. http://dx.doi.org/10.1071/rd20115.
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The menstruating Egyptian spiny mouse has recently been proposed as a new animal model for reproductive health research. Unfortunately, little is known about reproduction in males. This study compared several characteristics of sperm function before and after cryopreservation. Epididymal spermatozoa were cryopreserved in different concentrations of raffinose and skim milk and tested for motility and membrane integrity (Experiment 1). Further evaluations of motility, plasma membrane and acrosome integrity, mitochondrial membrane potential and DNA integrity were conducted with the addition of l-glutamine to the extender (Experiment 2). The results show that, following cryopreservation, motility and membrane integrity were reduced, but were better maintained in the presence of l-glutamine (P<0.05). Moreover, although all sperm parameters were significantly reduced following cryopreservation (P<0.05), most cryopreserved spermatozoa retained acrosome, membrane and DNA integrity while also maintaining motility and mitochondrial membrane potential. This study provides a new step towards the development of assisted reproductive techniques and archiving the important genetics of the world’s only known menstruating rodent.
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Lee, Sungeun, Dong-Wook Kang, Susan Hudgins-Spivey, Andree Krust, Eun-Young Lee, Youngbum Koo, Yongpil Cheon, Myung Chan Gye, Pierre Chambon, and CheMyong Ko. "Theca-Specific Estrogen Receptor-α Knockout Mice Lose Fertility Prematurely." Endocrinology 150, no. 8 (May 7, 2009): 3855–62. http://dx.doi.org/10.1210/en.2008-1774.
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Estrogen receptor-α (Esr1) mediates estrogen action in regulating at all levels of the hypothalamic-pituitary-ovarian axis. Whereas the importance of Esr1 in hypothalamus and pituitary has been demonstrated by loss of fertility in the neuron- and pituitary-specific Esr1 knockout mice, whether Esr1 plays a critical role in the ovary remains to be determined. In the ovary, Esr1 is mainly expressed in the theca/interstitial cells and germinal epithelium and thus is believed to mediate estrogen action in these cells. In this study, we assessed the importance of Esr1 in the ovarian theca cells in regulating female reproduction. The Cre-LoxP approach was used to selectively delete the Esr1 gene in the theca cells, and the reproductive consequence of the deletion was measured. Adolescent theca-specific Esr1 knockout (thEsr1KO) mice (<4 months of age) are fertile and cycling. However, they begin to display an erratic pattern of estrous cycles and become infertile before they reach the age of 6 months. The ovaries of thEsr1KOmice (≥4 months) have fewer corpora lutea but more antral follicles than the age-matching wild-type mice. The numbers of 17-hydroxylase-expressing cells are largely increased in the interstitium of the thEsr1KO mouse ovary. Interestingly, whereas basal levels of serum testosterone and FSH were mildly elevated, LH level was either markedly lower or undetectable in the thEsr1KO mice. When superstimulated by exogenous gonadotropins, thEsr1KO mice released significantly fewer oocytes that wild-type littermates and developed multiple hemorrhagic cysts. Taken together, this study demonstrates that theca Esr1 plays a critical role in regulating female reproduction.
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Bera, Tapan K., and Ira Pastan. "Mesothelin Is Not Required for Normal Mouse Development or Reproduction." Molecular and Cellular Biology 20, no. 8 (April 15, 2000): 2902–6. http://dx.doi.org/10.1128/mcb.20.8.2902-2906.2000.
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ABSTRACT Mesothelin is a glycosylphosphatidylinositol-linked glycoprotein highly expressed in mesothelial cells, mesotheliomas, and ovarian cancer, but the biological function(s) of the protein is not known. We have analyzed the expression of the mouse mesothelin gene in different developmental stages and in various adult tissues by Northern hybridization. The 2.5-kb mesothelin transcript was detected in the mRNA of E 7.0, E 15.0, and E 17.0 stages of mouse development. In adult tissues the mesothelin gene was expressed in lung, heart, spleen, liver, kidney, and testis. To directly assess the function of the mesothelin in vivo, we generated mutant mice in which the mesothelin gene was inactivated by replacing it with the neomycin resistance gene. In homozygous mutant mice neither mesothelin mRNA nor the protein product was detected. Null mutant mice were obtained in accordance with Mendelian laws, and both males and females produced offspring normally. No anatomical or histological abnormalities were detected in any tissues where mesothelin was reportedly expressed in wild-type mice. Our results demonstrate that mesothelin function is not essential for growth or reproduction in mice.
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Starobor, N. N., and O. V. Raskosha. "Reproductive parameters in Аf mice after chronic low-dose gamma radiation." Proceedings of the Komi Science Centre of the Ural Division of the Russian Academy of Sciences 5 (2021): 20–28. http://dx.doi.org/10.19110/1994-5655-2021-5-20-28.
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The results of the study of reproductive parameters in Af mice after chronic low-intensity γ-radiation at doses of 10, 20 and 30 cGy are presented. Males and females of the experimental groups were exposed to external γ-radiation (0.474x106 and 0.451x106 kBq226Ra) for 29, 56 and 84 days, at an average dose rate of 150 µSv/h. Immediately after the end of radiation exposure, pairs for animal reproduction were formed in the experimental and control groups. During the next three months, the number of females participating in reproduction, the number of litters and the number of cubs born were recorded in each group, and the early postnatal mortality of cubs (F1) was also estimated. In addition, radiation effects in male germ cells were studied 4 months after the termination of radiation exposure. The obtained results showed an increase in the number of cubs per female (at doses of 10–30 cGy) and the number of cubs in the litter (at doses of 20 and 30 cGy). It should be noted that the number of cubs in litters increased in females fertilized in the first 2-3 days after the end of radiation exposure, while after fertilization of females 40 or more days after irradiation, no statistically significant differences with the control group were found. The effect of stimulation in the germ cells of males was manifested in an increased content of spermatozoa in the epididymis of animals after radiation exposure at a dose of 30 cGy. An increase in the early postnatal mortality of cubs (F1) was detected in parents exposed to doses of 20 and 30 cGy, however, the reproductive index calculated taking into account the surviving cubs for the first month of life confirms the stimulating effect of ionizing radiation in the studied dose range on the fertility of animals.
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Hou, SY, L. Zhang, K. Wu, and L. Xia. "Thioglycolic acid inhibits mouse oocyte maturation and affects chromosomal arrangement and spindle configuration." Toxicology and Industrial Health 24, no. 4 (May 2008): 227–34. http://dx.doi.org/10.1177/0748233708095862.
Full textAbstract:
Previous studies have shown that thioglycolic acid (TGA) leads to potential reproductive toxicology. To clarify the exact effects of this compound on reproduction, mice oocytes were treated with different TGA doses. At the end of the culture period, the nuclear status of mice oocytes was assessed under an inverted microscope. After immunofluorescence staining, the chromosomal arrangement and spindle configuration of oocytes were evaluated. The results indicated that TGA decreases the percentage of first polar body formation but does not influence that of germinal vesicle breakdown. TGA induces abnormal chromosomal arrangement and spindle elongation. In conclusion, TGA inhibits in-vitro maturation of mice oocytes and affects chromosomal arrangement and spindle configuration. Furthermore, it probably interferes with biochemical changes that occur during meiosis, resulting in aberrant development.
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De Bond, Julie-Ann P., and Jeremy T. Smith. "Kisspeptin and energy balance in reproduction." REPRODUCTION 147, no. 3 (March 2014): R53—R63. http://dx.doi.org/10.1530/rep-13-0509.
Full textAbstract:
Kisspeptin is vital for the neuroendocrine regulation of GNRH secretion. Kisspeptin neurons are now recognized as a central pathway responsible for conveying key homeostatic information to GNRH neurons. This pathway is likely to mediate the well-established link between energy balance and reproductive function. Thus, in states of severely altered energy balance (either negative or positive), fertility is compromised, as isKiss1expression in the arcuate nucleus. A number of metabolic modulators have been proposed as regulators of kisspeptin neurons including leptin, ghrelin, pro-opiomelanocortin (POMC), and neuropeptide Y (NPY). Whether these regulate kisspeptin neurons directly or indirectly will be discussed. Moreover, whether the stimulatory role of leptin on reproduction is mediated by kisspeptin directly will be questioned. Furthermore, in addition to being expressed in GNRH neurons, the kisspeptin receptor (Kiss1r) is also expressed in other areas of the brain, as well as in the periphery, suggesting alternative roles for kisspeptin signaling outside of reproduction. Interestingly, kisspeptin neurons are anatomically linked to, and can directly excite, anorexigenic POMC neurons and indirectly inhibit orexigenic NPY neurons. Thus, kisspeptin may have a direct role in regulating energy balance. Although data fromKiss1rknockout and WT mice found no differences in body weight, recent data indicate that kisspeptin may still play a role in food intake and glucose homeostasis. Thus, in addition to regulating reproduction, and mediating the effect of energy balance on reproductive function, kisspeptin signaling may also be a direct regulator of metabolism.