The Regulation Of Cholesterol And Lipid Homeostasis

Figure 1 [2]: The role of tubules in cell proliferation and differentiation of sperm cells.

Blog Male birth control pill moves a step closer16th August 2012Researchers have finally found a compound that may offer the first effective and hormone-free birth control pill for men.The study, published today in the journal Cell, describes how the small molecule makes male mice reversibly infertile, without putting a damper on their sex drive. When the animals stop taking this new form of birth control, their sperm rebound and they are able to produce perfectly healthy offspring once again."This compound produces a rapid and reversible decrease in sperm count and motility with profound effects on fertility," said James Bradner of the Dana-Farber Cancer Institute and lead author of the study.A male birth control

Recently there has been a trail study on a shot that could be a new form of birth control for males, it contains progestin and testosterone and needs to be taken every two months. The film Male Pill by ABC International explained more about the study apparently “it has to be through a shot because orally the testosterone can be broken down by the liver.” It explained how the male body worked before and after the use of the shot. ABC International said:

The male reproductive system is effect by the cause of oligospermia and azoospermia, decreased the testicular size, abnormal appearance of testicular biopsy material, and reductions in testosterone and gonadotropic hormones. The change in the body seen in the pituitary-gonadal which leads to the suppression of gonadotrophin production. The variations in these hormones can alter thyroid function and negative impact on glucose tolerance. The Abuse of steroids affects the male reproductive be reversible with cessation of steroid that can cause, although breast tissue changes and hair loss. It can lead to surgery needs of an

State the chemical composition of the sterol that is present in high levels in most people who belong to the high-risk group.

Nevertheless, like humans, the animal samples showed that androgens alone are sufficient to the induction of prostate carcinogenesis. In this study, the mean age of the patients who were sample was about 63 years of age and the median time that it took to diagnose those patients was almost three years. Testosterone, in this study, was moderately correlated with SHBG, but weakly correlated with estradilol. This is when Black et al used the ratio of estradilol: testosterone because they found an decrease between the ratio and the risk of acquiring prostate cancer. The overall conclusion was acquired from the data was found what that in men 70 years of age or greater a higher ratio of estradilol: testosterone was strongly associated with a reduced risk, and the control of the ratio would reduce the risk of acquiring prostate cancer. The risk of having prostate cancer was observed as higher with a ratio of 2:16α-hydroxyestrone. Even though it was found that there is low risk of getting prostate cancer, they did consider the balance is important in how aggressive the prostate cancer is, or may become. [4]

Cholesterol, like fat, cannot move around the bloodstream on its own because it does not mix with water. The bloodstream carries cholesterol in particles called lipoproteins that are like blood-borne cargo trucks delivering cholesterol to various body tissues to be used, stored or excreted. But too much of this circulating cholesterol can injure arteries, especially the coronary ones that supply the heart. This leads to accumulation of cholesterol-laden “plaque” in vessel linings, a condition ca

Females did not appear to conserve a minimum number of spermatophores for future fertilizations when eating spermatophores (number of spermatophores after consumption: minimum = 8, maximum = 35, range = 27), with no increase in consumption when males invested heavily (controlled for female size: F1,15 = 3.53, P = 0.079). Male size had no effect on female spermatophore consumption (linear regression: R2 = 0.023, P =

Both animal and clinical studies have demonstrated that obesity leads to ovarian dysfunction through oxidative and ER stress and inflammation (26,65,66,74-78). Obesity leads to excess lipids, glucose, insulin, and leptin in variety of ovarian cells including: granulosa cells, cumulus cells, oocytes, and early embryos (ref more;(65,79,80)). Because leptin contributes to follicular growth, steroidogenesis, oocyte maturation and embryo development, hyperleptinemia seen in obese women may disrupt these processes (30,58,70,75,78,81-96). Similarly, insulin resistance and or hyperinsulinemia, have been shown to alter ovarian morphology, ovarian insulin signaling, ovulation and maturation of oocytes (23,30,36,39,40,71,73,74,97-107). Obesity leads to elevated levels of circulating lipids as well as lipid accumulation in the ovary which are associated with decreased granulosa cell numbers, increased apoptosis, greater lipid accumulation in cumulus cells, decreased oocyte nuclear maturation, and changes in substrate metabolism and proliferation in embryos (18,36,55,63,65,67,75,79,90,92,108-112). Greater oxidative stress and chronic low grade inflammation, as seen in obese animals and humans, have also been shown to alter oocyte maturation and fertilization, embryo development and pregnancy success (19,26,65,66,68,69,74,77,78,104,105,109,110,113-120). Lastly, obesity leads to a variety of oocyte mitochondrial defects, including

As soon as sperm cells are deposited in the female reproductive tract and pass the cervical mucus, they undergo many biochemical and physiological changes, including changes in the pattern of sperm motility known as hyperactivation, and the sperm become competent to fertilize an oocyte, in a process called capacitation 21,22. The biochemical changes that occur in this process include an efflux of cholesterol from the plasma membrane leading to an increase in membrane fluidity and permeability to bicarbonate and calcium ions which results in an increase in bicarbonate (HCO3-) concentration and intracellular pH, Ca2+, and cyclic adenosine monophosphate (cAMP) levels. 4,23.

1.Cholesterol functions as the important precursor molecule for the synthesis of the steroid hormones in animal bodies, including the sex hormones.

Furthermore, there was a study conducted in 2013 that showed another msx1 function in dairy goat male. Msx1 enhanced the expression of Stra8, germline gene, and Scp3, synaptonemal complex protein, and promote the meiosis in goat testicular cells. It was proven n vitro Bmp4 and retinoic acid, RA promote the expression of Msx1 in mice testis(8).

Spermatogenesis is the 65 to 75 day process in which the human male anatomy produces sperm cells. In the male body, follicle-stimulating hormones, or FSH, and leutinizing hormones, or LH, are very important in the process of spermatogenesis. These hormones control sperm reproduction. The production of the hormones testosterone and androgens are stimulated

The foetal Leydig Cell population arises shortly after testicular differentiation around 7 weeks in a human after gestation by the Human Chorionic Gonadotropin (hcG), this is known as the first wave (45). These cells function, mainly to produce androgens which are essential for masculinization of the foetus as well as in the descent of the testes in the scrotum, these androgens subsequently act as paracrine factors within the seminiferous tubules, testosterone, is only first detected around 6-7 weeks of gestation and peaks around 13-14 weeks (45). In cases where Leydig cells fail to develop or fail to produce androgens, pseudohermaphrodism occurs (46). The androgen produced ensures the Wolffian duct is maintained and there is

Leydig cells have essential roles in the maintenance of steroidogenesis and spermatogenesis in the testes. The failures of both processes are attributed to Leydig cell dysfunction. In the current research, expression of testicular LH receptor and FSH receptor mRNAs was significantly lower in the treated ram lambs (P < 0.05), implying that testicular responsiveness to LH stimulation was impaired. Indeed, active immunization against GNRH in boars significantly reduced testicular LH receptor and testosterone concentrations following treatment with exogenous LH [Wei et al. 2011; Wei et al., 2012]. Moreover, expression of testicular LHR mRNA was significantly decreased, which further confirmed that the functions of Leydig within testes were severely impaired. In addition, it is well known that FSH plays a role in spermatogenesis. However, the expression levels of FSHR mRNA in the testes of treated rams and control rams were not siginificantly different, demonstrating oral kisspeptin DNA immunization has no influence on