scholarly journals Physiologic Course of Female Reproductive Function: A Molecular Look into the Prologue of Life

2015 ◽  
Vol 2015 ◽  
pp. 1-21 ◽  
Author(s):  
Joselyn Rojas ◽  
Mervin Chávez-Castillo ◽  
Luis Carlos Olivar ◽  
María Calvo ◽  
José Mejías ◽  
...  

The genetic, endocrine, and metabolic mechanisms underlying female reproduction are numerous and sophisticated, displaying complex functional evolution throughout a woman’s lifetime. This vital course may be systematized in three subsequent stages: prenatal development of ovaries and germ cells up untilin uteroarrest of follicular growth and the ensuing interim suspension of gonadal function; onset of reproductive maturity through puberty, with reinitiation of both gonadal and adrenal activity; and adult functionality of the ovarian cycle which permits ovulation, a key event in female fertility, and dictates concurrent modifications in the endometrium and other ovarian hormone-sensitive tissues. Indeed, the ultimate goal of this physiologic progression is to achieve ovulation and offer an adequate environment for the installation of gestation, the consummation of female fertility. Strict regulation of these processes is important, as disruptions at any point in this evolution may equate a myriad of endocrine-metabolic disturbances for women and adverse consequences on offspring both during pregnancy and postpartum. This review offers a summary of pivotal aspects concerning the physiologic course of female reproductive function.

2017 ◽  
Vol 29 (7) ◽  
pp. 1426 ◽  
Author(s):  
K. A. Walters ◽  
M. C. Edwards ◽  
M. Jimenez ◽  
D. J. Handelsman ◽  
C. M. Allan

Androgens synergise with FSH in female reproduction but the nature of their interaction in ovarian function and fertility is not clear. In the present study, we investigated this interaction, notably whether higher endogenous FSH can overcome defective androgen actions in androgen receptor (AR)-knockout (ARKO) mice. We generated and investigated the reproductive function of mutant mice exhibiting AR resistance with or without expression of human transgenic FSH (Tg-FSH). On the background of inactivated AR signalling, which alone resulted in irregular oestrous cycles and reduced pups per litter, ovulation rates and antral follicle health, Tg-FSH expression restored follicle health, ovulation rates and litter size to wild-type levels. However, Tg-FSH was only able to partially rectify the abnormal oestrous cycles observed in ARKO females. Hence, elevated endogenous FSH rescued the intraovarian defects, and partially rescued the extraovarian defects due to androgen insensitivity. In addition, the observed increase in litter size in Tg-FSH females was not observed in the presence of AR signalling inactivation. In summary, the findings of the present study reveal that FSH can rescue impaired female fertility and ovarian function due to androgen insensitivity in female ARKO mice by maintaining follicle health and ovulation rates, and thereby optimal female fertility.


Reproduction ◽  
2018 ◽  
Author(s):  
Susana B Rulli ◽  
María Julia Cambiasso ◽  
Laura D Ratner

In mammals, the reproductive function is controlled by the hypothalamic-pituitary-gonadal axis. During development, mechanisms mediated by gonadal steroids exert an imprinting at the hypothalamic-pituitary level, by establishing sexual differences in the circuits that control male and female reproduction. In rodents, the testicular production of androgens increases drastically during the fetal/neonatal stage. This process is essential for the masculinization of the reproductive tract, genitals and brain. The conversion of androgens to estrogens in the brain is crucial for the male sexual differentiation and behavior. Conversely, feminization of the brain occurs in the absence of high levels of gonadal steroids during the perinatal period in females. Potential genetic contribution to the differentiation of brain cells through direct effects of genes located on sex chromosomes is also relevant. In this review, we will focus on the phenotypic alterations that occur on the hypothalamic-pituitary-gonadal axis of transgenic mice with persistently elevated expression of the human chorionic gonadotropin hormone (hCG). Excess of endogenously synthesized gonadal steroids due to a constant hCG stimulation is able to disrupt the developmental programming of the hypothalamic-pituitary axis in both transgenic males and females. Locally produced estrogens by the hypothalamic aromatase might play a key role in the phenotype of these mice. The “four core genotypes” mouse model demonstrated a potential influence of sex chromosome genes in brain masculinization before critical periods of sex differentiation. Thus, hormonal and genetic factors interact to regulate the local production of the neurosteroids necessary for the programming of the male and female reproductive function.


Reproduction ◽  
2018 ◽  
Vol 155 (4) ◽  
pp. R169-R181 ◽  
Author(s):  
K L Bidne ◽  
M J Dickson ◽  
J W Ross ◽  
L H Baumgard ◽  
A F Keating

Endotoxemia can be caused by obesity, environmental chemical exposure, abiotic stressors and bacterial infection. Circumstances that deleteriously impact intestinal barrier integrity can induce endotoxemia, and controlled experiments have identified negative impacts of lipopolysaccharide (LPS; an endotoxin mimetic) on folliculogenesis, puberty onset, estrus behavior, ovulation, meiotic competence, luteal function and ovarian steroidogenesis. In addition, neonatal LPS exposures have transgenerational female reproductive impacts, raising concern about early life contacts to this endogenous reproductive toxicant. Aims of this review are to identify physiological stressors causing endotoxemia, to highlight potential mechanism(s) by which LPS compromises female reproduction and identify knowledge gaps regarding how acute and/or metabolic endotoxemia influence(s) female reproduction.


Cephalalgia ◽  
1997 ◽  
Vol 17 (20_suppl) ◽  
pp. 12-16 ◽  
Author(s):  
Kma Welch

This chapter reviews clinical and epidemiological data that support a role for ovarian steroid hormones in the migraine syndrome. Changes in the clinical presentation of migraine are discussed on the basis of current knowledge of biochemistry and pharmacology of ovarian steroids. Finally, special treatment considerations of ovarian hormone-sensitive migraine are discussed.


Endocrinology ◽  
2000 ◽  
Vol 141 (12) ◽  
pp. 4777-4783 ◽  
Author(s):  
Joy Y. Wu ◽  
Ignacio J. Gonzalez-Robayna ◽  
JoAnne S. Richards ◽  
Anthony R. Means

Abstract Ca2+/calmodulin-dependent protein kinase IV (CaMKIV) is a serine/threonine protein kinase with limited tissue distribution. CaMKIV is highly expressed in the testis, where it is found in transcriptionally inactive elongating spermatids. We have recently generated mice deficient in CaMKIV. In the absence of CaMKIV, the exchange of sperm nuclear basic proteins in male spermatids is impaired, resulting in male infertility secondary to defective spermiogenesis. The involvement of CaMKIV in female fertility has not been addressed. Here we report that female fertility is markedly reduced in CaMKIV-deficient mice due to impaired follicular development and ovulation. CaMKIV is expressed in the ovary, where it is localized in granulosa cells. We further find that in cultured granulosa cells, CaMKIV expression and subcellular localization are hormonally regulated. As granulosa cells differentiate, CaMKIV levels decrease and the kinase translocates from the nucleus into the cytoplasm. Our results demonstrate a critical role for CaMKIV in female reproduction and point to a potential function in granulosa cell differentiation.


1999 ◽  
Vol 24 ◽  
pp. 99-112 ◽  
Author(s):  
R. Webb ◽  
P. C. Garnsworthy ◽  
J. G. Gong ◽  
R. S. Robinson ◽  
D. C. Wathes

AbstractAn effective method for enhancing milk production efficiency in dairy cows is to increase milk yield and significant progress has been achieved through intense selection, assisted by the application of new reproductive techniques. However this increased milk yield has been accompanied by a slow but steady decline in dairy cow fertility. The two main reasons for this reducing level of fertility appear to be selection for increased milk yield and large herd sizes, although the affect of the introduction of Holstein genes needs to be investigated. In addition, other negative consequences such as an increase in the incidence of metabolic diseases and lameness have been observed. This has given rise to public concern that the high-yielding dairy cow may be under a state of metabolic stress during peak lactation and therefore the welfare and performance of other body functions are compromised.The reason for this decline in fertility is not well understood, although a nutritional influence on the initiation of oestrous cycles, follicular growth, oocyte quality and early embryonic development has been implicated. In early lactation dietary intake is unable to meet the demands of milk production and most cows enter a period of negative energy balance. Negative energy balance has a broadly similar effect to undernutrition leading to a mobilization of body reserves. Furthermore diets high in rumen degradable protein lead to an excess of rumen ammonia, which before it is converted to urea by the liver and excreted in the urine, may cause an alteration in the reproductive tract environment reducing embryo survival. Such major changes in the metabolic and endocrine systems can therefore influence fertility at a number of key points.Possible reproductive sites where inadequate nutrition may have detrimental effects include: (i) the hypothalamic/pituitary gland where gonadotropin release may be impaired; (ii) a direct effect on the ovaries, where both follicular growth patterns and corpus luteum function may be directly influenced; (iii) the quality of the oocyte prior to ovulation may be reduced and coupled with an inadequate uterine environment will result in reduced embryo survival and (iv) there may be effects on subsequent embryo development. The initiation of normal oestrous cycles post partum is usually delayed in dairy cows with a higher genetic merit for milk production, confirming that intense selection towards high milk yield can compromise reproductive function. In addition, the effects of increased milk yield may include changes in circulating GH and insulin concentrations, which in turn alter both insulin-like growth factor (IGF) and IGF binding protein production. Nutrition has recently been shown to have a direct effect at the level of both the ovaries and the uterus to alter the expression of these growth factors.In conclusion, further knowledge is required to determine how the metabolic changes associated with high milk output reduce fertility. Identification and understanding of the mechanisms involved and the key sites of action responsible for compromised reproductive function, will enable the identification of possible indices for future multiple-trait selection programmes.


Endocrinology ◽  
2019 ◽  
Vol 161 (1) ◽  
Author(s):  
Djurdjica Coss

Abstract Follicle-stimulating hormone (FSH) is a dimeric glycoprotein secreted by the anterior pituitary gonadotrope that is necessary for reproductive function in mammals. FSH primarily regulates granulosa cells and follicular growth in females, and Sertoli cell function in males. Since its identification in the 1930s and sequencing in the 1970s, significant progress has been made in elucidating its regulation and downstream function. Recent advances provide deeper insight into FSH synthesis, and effects in the gonads suggest potential roles in extragonadal tissues and examine pharmacological approaches and clinical applications in infertility treatment that now affect 18% of couples. These advances were discussed in detail in a number of reviews published in the last 2 years in Endocrinology. In this brief commentary, we summarize these reviews and point to the outstanding questions that should be answered in the near future to bridge a gap in our understanding of this hormone.


2017 ◽  
Vol 15 (3) ◽  
pp. 5-21 ◽  
Author(s):  
Elena V. Stashina ◽  
Nikolay A. Gavrilov ◽  
Petr D. Shabanov

Environmental toxicants, chemicals exhibiting with cholinotropics properties, and drugs – agonists and antagonists of M- and N-cholinergic receptors by acting on the developing brain of the fetus in the embryonic period of ontogenesis, cause a change the activity of the cholinergic mechanisms of the brain during critical periods of prenatal development with the subsequent disruption of the formation of different brain systems, primarily the ontogeny of nerve cells and brain neurotransmitter systems. These changes in the long term is correlated with neurobehavioral deficits from adult individuals, dysfunction of the reproductive system of adult offspring. The relevance of the study of prenatal effects of cholinergic factors on the central mechanisms of reproductive function, memory processes and learning during ontogenetic development of the organism due to the need of prevention and treatment of subsequent mental, behavioral, and sexual dysfunctions, and abnormal sexual behavior, infertility.


Author(s):  
Petr Petrovich Geraskin ◽  
Angelika Vyachislavovna Kovaleva ◽  
Vadim Alekseevich Grigoriev ◽  
Angelina Valerievna Firsova ◽  
Marina Yaitskaya ◽  
...  

The article highlights the problem of significant reducing the number of beluga at the beginning of the XXI century, which resulted in restoring its population artificially. The formation of repair and brood stocks is slowing down due to a significant shortage of producers of natural generation. Artificial reproduction of beluga is currently carried out due to domestication of fish, as well as by growing mature individuals on “from eggs to eggs” principle. Producers grown in the hatcheries often have metabolic disturbances, signs of physiological exhaustion, and a modified biochemical composition of oocytes. All these deteriorate the reproductive functions of the producers. There have been presented the results of studying physiological preparedness of beluga producers to spawning campaign carried out by the Caspian branch FSBO “Glavrybvod” at the Sergievsky sturgeon hatchery. The objects of the study were females caught in the natural environment and domesticated in the hatchery, as well as sixteen-eighteen-year-old females from their own broodstock. Physiological readiness for spawning was assessed by a complex of physiological and biochemical parameters of blood and the amount of accumulated plastic and energy substances in oocytes in the form of proteins and lipids. It was revealed that domesticated females were better prepared for pituitary injections than females from the broodstock. This was justified by both physiological and biochemical parameters, as well as by the coefficient of polarization of oocytes. Eggs of females grown in the hatchery conditions are smaller (1.3 times smaller) and the number of triglycerides in them is 4.35 times less than in those of domesticated fish. In addition, the accumulation of protein and lipids by oocytes differs greatly in broodstock female species due to heterogeneity of their functional state.


Reproduction ◽  
2019 ◽  
Vol 157 (3) ◽  
pp. 305-316 ◽  
Author(s):  
Vijay Pratap Singh ◽  
Wei-Ting Yueh ◽  
Jennifer L Gerton ◽  
Francesca E Duncan

Eighteen histone deacetylases exist in mammals. The class 1 histone deacetylases HDAC1 and HDAC2 are important for oogenesis and fertility in mice, likely via their effects on histones. The reproductive function of HDAC8, another class 1 enzyme, has not been explored. One key target of HDAC8 is the SMC3 subunit of cohesin, an essential complex mediating sister chromatid cohesion and chromosome segregation. In current models, HDAC8 activity is required for SMC3 recycling, but this function should be dispensable in oocytes since cohesion is established during pre-meiotic S phase and maintained until meiotic resumption during ovulation. Whether other oocyte-specific HDAC8-mediated deacetylation events are required for oogenesis and female fertility is unknown. We used two Cre drivers to remove Hdac8 at specific stages of oocyte development to address whether HDAC8 is required for female fertility in mice. When HDAC8 was knocked out in oocytes in primary and later stage follicles (Zp3-Cre), oogenesis and folliculogenesis appeared normal and mice were fertile. However, females were subfertile when HDAC8 was knocked out prior to pre-meiotic S phase and cohesion establishment (Vasa-Cre). This subfertility was independent of chromosome segregation errors during meiosis but rather appeared to be the result of defects in oogenesis that resulted in smaller fully grown oocytes with a reduced ability to resume meiosis. In all cases, we did not observe compensatory changes in HDAC1, HDAC2 and HDAC3 levels. Thus, although oocyte-specific expression of HDAC8 is not essential for mouse oogenesis after meiotic S phase, it contributes to optimal fertility. We infer that oocyte-specific expression of the deacetylase HDAC8 is required early in oogenesis for optimal fertility.


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