Women are more prone to infertility
Women are more prone to infertility
Women are more prone to infertility
WOMENARE MORE PRONE TO INFERTILITY.
By Prof G .M.Wani, PhD,DVM (Germany)
Mother's obesity may lead to daughters infertility. Levels of the hormone ghrelin are low in obese women. The mice from low ghrelin levels were less fertile due to a defect in implantation. The said hormone which infect is a factor for maintenance of energy balance and metabolism principally, also plays a role in reproductive function too. This paper reviews the effect of ghrelin deficiency on female infertility.
The investigations on mice reveal that obese mother uterus is not able to develop the female offspring properly .Perhaps its uterus development remains defective such that at puberty it leads to infertility(Taylor,2011) Female Germ cells and cancer therapy Male germ cells are produced throughout the whole life span but the number of female germ cells is restricted and slower. If the oocytes are damaged during cancer treatment, they are destroyed by the female's own internal quality control system. The female germ cell number is fixed at birth. Male spematogonia cell are continuously produced and regenerated throughout the life of the male reproductive life.
This is why even if a male is subjected to radiotherapy his germ cell even if damaged can recover as next generation spermatogonia may be formed and could be free of radiation damage. I have seen many males treated with radiation at Tata memorial Hospital and they recovered. I know two of them Dr MA ZAKI ,Prof of Entomology at SKUAST-K and DR Mumtazudin a surgeon specialist at SMHSH ,Hospital.Srinaagr who have been bestowed with children after radiation therapy.It was a blessed and most wished gift of God to them,as both have sons after radiation therapy which they longed for long as both had two daughters ech before therapy..
Thus radiation therapy in male has a way to avoid infertility, but it is as on today different and difficult but not impossible for a female partner or women.My hypothsis is as . The recent investigations that even surface epithelium of the ovary have a potential to be precursor of stem cells which if reared properly may give rise to germ cells .Second the response of resting follicle to be used for invitro maturation in the life of a female new born at later stage gives a hope to cure infertility in them even after cancer therapy destroys their capacity to produce viable oocyte.
Essential to that process is the protein p63 which shows striking similarity to another important protein of the same family - p53. The protein p53 is called the "guardian of the genome" because it regulates the function of cell division and cell death in damaged cells. It suppresses genetic irregularities which could lead to cancer. In more than half of all human tumors p53 is altered and no longer functioning. Tetramer formation For a long time p53 and p63, their similarities and differences, have been studied in international research. It is currently accepted that healthy cells have a low concentration of p53. But gene anomalies break the DNA chain and reform its strands, p53 changes into a tetramer. In this state it becomes active and initiates either repair of the damaged DNA or promote cell death.
Surprisingly, despite the fact that p53 and p63 show a lot of similarity, control of p63 in oocytes seems to be different. The level of p63 in normal oocytes is high and the protein is kept in a closed dimeric - or inactive state. If DNA double-strand breaks occur, for example caused by radiation, p63 becomes phosphorylated and its structure changes. The resulting p63 tetramer is similar to the p53 tetramer and leads to the death of the oocyte. Many chemo therapy agents cause DNA double-strand breaks in p63 and ultimately to the death of eggs. It is said that p63 is the investor of the entire family p53 .Interestingly, p63 is also essential for the maintenance of stem cells in epithelial skin cells. Because of the close similarity of stem cells and germ cells, this adds to the evidence for evolution of p63 into p53-like proteins, underlining the importance of the both proteins
GHERELIN HORMONE
It is observed that female mice born of mice with ghrelin deficiency had diminished fertility and produced smaller litters than mice born of mice with normal ghrelin levels. Mice exposed to ghrelin deficiency in-uteri demonstrated alterations in uterine gene expression which lead to impaired embryo implantation and consequently low fertility. Early in human embryo formation, a transcription factor called Twist! Plays a key role in regulating how the embryo assumes its form and function. However, much later in life twist! Turns more deadly. OBESITY AND IMPLANTATION Obese mothers have low levels of hormone gherelin Male germ cells are produced throughout the whole life span but the number of female germ cells is restricted and slower. If the oocytes are damaged during cancer treatment, they are destroyed by the female's own internal quality control system. Essential to that process is the protein p63 which shows striking similarity to another important protein of the same family - p53.
The protein p53 is called the "guardian of the genome" because it regulates the function of cell division and cell death in damaged cells. It suppresses genetic irregularities which could lead to cancer. In more than half of all human tumors p53 is altered and no longer functioning. For a long time p53 and p63, their similarities and differences, have been studied in international research. It is currently accepted that healthy cells have a low concentration of p53. But gene anomalies break the DNA chain and reform its strands, p53 changes into a tetramer. In this state it becomes active and initiates either repair of the damaged DNA or promote cell death. Surprisingly, despite the fact that p53 and p63 show a lot of similarity, control of p63 in oocytes seems to be different. The level of p63 in normal oocytes is high and the protein is kept in a closed dimeric - or inactive state. If DNA double-strand breaks occur, for example caused by radiation, p63 becomes phosphorylated and its structure changes.
The resulting p63 tetramer is similar to the p53 tetramer and leads to the death of the oocyte. Many chemo therapy agents cause DNA double-strand breaks in p63 and ultimately to the death of eggs. P63 does not act as a tumor suppressor but instead controls the eggs' genetic stability. This may have been the original function of the p53 protein - and leads to the speculation that p63 is the ancestor of the entire p53 family. Interestingly, p63 is also essential for the maintenance of stem cells in epithelial skin cells.
Because of the close similarity of stem cells and germ cells, this adds to the evidence for evolution of p63 into p53-like proteins, underlining the importance of the both proteins to human health.
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