Written by Ben Bunting: BA(Hons), PGCert.
The skeleton has many functions, one of which is endocrine regulation of male fertility. The skeletal muscles and endocrine system control energy metabolism in the body. Testosterone and Osteocalcin are two hormones that play a role in regulating fertility. But what happens when they are not present? How does testosterone influence male fertility? The skeleton controls testosterone and Osteocalcin production, which are necessary for both growth and reproduction.
There is a question regarding the mechanism of action of osteocalcin, a hormone secreted by osteoblasts. Identifying the receptor is the first step in determining its mechanism of action. Since osteocalcin only regulates male fertility, it is not clear how it works in females. However, its presence in the body may help explain how it regulates male fertility.
Studies in mice have shown that osteocalcin and testosterone levels have a direct relationship. The expression of osteocalcin is related to the activity of osteoclasts and testosterone levels. In these studies, osteocalcin and testosterone were measured in serum of WT and Opg-/ mice at ten, twelve, and twenty-two weeks of age. In addition, testes cross-sections were performed to determine the effects of osteocalcin and testosterone on male fertility.
Researchers have found that the hormone Osteocalcin promotes the production of testosterone, a key factor in male fertility. Testosterone supports the survival of germ cells, which develop into mature sperm. This study is the first evidence that the skeleton regulates reproduction. This discovery is intriguing, as it shows that male fertility is influenced by insulin signaling and bone resorption.
Although it is unclear whether this hormone is responsible for male fertility, it does play an important role in mouse reproduction. Interestingly, the hormone does not affect the expression of osteocalcin in human osteoblasts, which provides additional evidence that osteocalcin regulates the reproductive function of mice. In humans, it may be useful for patients with peripheral testicular failure. So, the research into the hormone may shed light on the role of the skeleton in male fertility.
The hormone testosterone is found in greater concentrations in men than in women. It initiates the development of the male reproductive organs during foetal development and is essential for the production of sperm in adult life. It also signals the body to produce new blood cells, maintains muscle and bone strength during puberty, and promotes libido in both sexes. Testosterone is also important in puberty, regulating the secretion of the follicle stimulating hormone and luteinising hormone.
The testis is the primary male reproductive organ and is important for spermatogenesis. It also secretes hormones, including gonadotropins. These hormones regulate the skeletal and reproductive functions of men. High levels of ROS disrupt this communication and impair reproduction. Testosterone acts as a hormone for the testis, and its metabolites enhance cellular antioxidants.
The first week of life is when testosterone levels are elevated. Testosterone affects the survival of germ cells, but it does not regulate the synthesis of estrogen. The skeleton does not favor estrogen synthesis in females, and peripheral organs may secrete hormones that promote estrogen synthesis. Testosterone also affects the formation of estradiol.
Similarly, CrebLeydig-/ mice show lower levels of male fertility, whereas CrebLeydig+/ mice have reduced sperm counts. This difference between the two groups of mice is striking, and is likely the reason why CrebLeydig-/ mice are so fertile. Although CrebLeydig-/ mice have reduced fertility, the aforementioned mutations cause the reduced fertility of these mice.
There are two main branches of life-history: growth and defense. Biologically, they are opposite in nature, and the allocation of resources is dependent on the environment. Glucocorticoids, prototypical stress hormones, are catabolic and oppose the anabolic response. Although the biological function of osteocalcin is unclear, it is likely to contribute to male fertility regulation.
The osteocalcin hormone, which is expressed in osteoblasts, is thought to be responsible for regulating male fertility. This hormone binds to a specific receptor on the testis' Leydig cells, favoring testosterone biosynthesis. These results support the hypothesis that regulation of bone remodeling is related to energy metabolism and reproduction, and that bone is a more important regulator of whole-organ physiology than previously thought.
The discovery of endocrine mediators produced by the skeleton has radically transformed the field of bone biology and endocrinology. In the past, textbooks have posited that the endocrine axis consists of the hypothalamus, pituitary, and endocrine gland. But the skeleton is now recognized as an integral part of endocrine function, integrating sensing, tropism, testosterone synthesis, and glandular effector function.
A hormone called osteocalcin is a possible drug target for male infertility. This hormone increases the production of testosterone, a sex steroid hormone that controls male fertility. Osteocalcin works by adding to cells that produce testosterone, increasing the level of testosterone and enhancing the reproduction of male mice. Researchers plan to study the signaling pathways that osteocalcin uses to enhance testosterone production. A drug targeting this receptor may give researchers more flexibility in the development of compounds.
Bone is often thought of as a simple, inert calcified tube, but this notion is no longer valid. Bone has developed into a bona fide endocrine organ with links to energy metabolism and reproduction. Previous studies of skeletal ties to reproduction focused on reproductive organs. Researcher's wondered if this influence could work the other way as well. Since women are more likely to develop osteoporosis, they expected that bone remodeling would be more common in females.
The study also extends previous research into the role of osteocalcin in the skeleton in regulating male fertility. The research provides important evidence that the skeleton plays a key role in regulating reproductive function. The study will appear in the journal Cell on February 17 and in the print edition on March 4.
A growing number of studies on male fertility have been motivated by reports of declining semen quality and decreased fertility rates. Several factors have been linked to the production of reactive oxygen species (ROS), or highly reactive oxygen derivatives with nano or millisecond half-lives. In addition to increased pollution, lifestyle modifications, and technological developments are among the chief exogenous sources of ROS.
Hormones mediating endocrine functions of bone
The regulation of male fertility by osteocalcin is pituitary and bone-dependent, raising the question of upstream regulators. Osteocalcin is important for favoring glucose homeostasis and bone resorption affects male fertility. The resorption of bone has been linked to the production of testosterone. However, how osteocalcin activates testosterone production in the testicles remains unclear.
Although bone is not a reproductive organ, research on this hormone has been ongoing since it was recognized as a hormone in rodents and identified as a regulatory factor in testosterone production in humans. Studies have shown a relationship between testosterone and serum osteocalcin levels during male mid-puberty. Such a relationship may be relevant during the rapid growth of the skeletal system during the adolescent years.
The importance of osteocalcin to male fertility has long been suspected. The hormone regulates sperm production, insulin secretion, and glucose homeostasis. It is also a reliable indicator of testosterone circulating in the blood, which may be relevant to humans. In addition, osteocalcin also has implications in identifying the susceptibility locus for primary testicular failure.
Previous studies have indicated that osteocalcin influences the growth and development of bone. In male mice, osteocalcin-null animals develop reproduction phenotypes in the presence of increased LH. This suggests that osteocalcin has a dual role in male fertility, regulating both pituitary and bone-based sex steroid synthesis. These findings underscore the notion that the skeleton is an endocrine organ and may have other important roles.