Summary: The Kisspeptin-Kiss1r System

The gonads are the male and female reproductive organs, the testes (males) and ovaries (females). The testes and ovaries produce androgens (testosterone) and estrogens, these hormones affect aggressiveness, mood, and sexual interest and behavior. Higher levels of these hormones have been shown to promote aggressiveness in both sexes (Morris and Maisto, 2002).

This complex organ can be found in upper right side of the abdomen. It is unique because it is a dual functioning organ. The first function is to control the body’s blood sugar level. The second function is to secrete insulin and glucagon. Lastly, I studied the testes of the fetal pig, which I found at the end of the scrotum under the skin. The teste are a key part in the process of secreting testosterone. After completing this section I began to dissect the last system of the pig.

The hypothalamus produces hormones that travel in blood vessels to the anterior pituitary, stimulating it to produce other hormones.

In the female reproductive system a hormone known as estrogen is controlled by gonadotropin which is controlled by negative feedback. During negative feedback from the estrogen prevent the anterior pituitary gland

to produce hormones that are beneficial to the activation of others parts of the brain and body. (Berger 201, pgs. 217-219)

The pituitary gland in the middle of the brain sends hormone signals to the testis to make them secrete testosterone, which stimulates sperm production. The challenge is to stop the sperm production, but maintain testosterone levels. When the shot of testosterone and progestin is injected a signal is sent to the pituitary gland fooling it in thinking the testis are producing sperm as a result both sperm and testosterone production are shut down. That’s when the injected testosterone kicks in bringing a man’s levels back to normal.

Luteinizing hormone releasing hormone (LHRH) agonists therapy may be used to enhance a negative feedback loop between the anterior pituitary and testicles, thus inhibiting the production of TST. LHRH agonists replicate the effects of endogenous luteinizing hormone which cause an acute rise in TST production — followed by a significant decrease in long term TST levels. LHRH antagonists may be used to disrupt the hypothalamic pituitary axis and inhibit the production of male sex androgens. The therapeutical index of LHRH antagonists may be greater than that of LHRH agonists because they do not cause the acute flare in TST as

The next study was conducted by Michael G. Dupree et al. in the year of 2003,  where they studied to see if the gene, Aromatase cytochrome P450 (CYP19), affected sexual orientation during development since it changes the levels of androgens and estrogens. Studies have shown that developing male brains are sexually altered by the hormones secreted by the fetal testes (DuPree et al., 2003). The ratio Androgen to estrogen plays an important role when it comes to developing the masculinization of the fetal brain (DuPree et al., 2003). The results of the study indicated that CYP19 did play a role in developing sexual orientation since it plays a key role in the sexual differentiation in the brain. They found more traces of CYP19 mRNA in homosexual

Greives, T. J., Long, K. L., Burns, C. M. B., & Demas, G. E. (2011). Response to Exogenous Kisspeptin Varies According to Sex and Reproductive Condition in Siberian Hamsters. (Phodopus sungorus). General and Comparative Endocrinology, 170, 172–179.

Biological differences between men and women contribute to many sex-specific illnesses and disorders. Historically, it was argued that such differences were largely, if not exclusively, due to gonadal hormone secretions. However, emerging research has shown that some differences are mediated by mechanisms other than the action of these hormone secretions and in particular by products of genes located on the X and Y chromosomes, which we refer to as direct genetic effects. Gonadal or sex hormones are steroids, they dominate the male sex hormone which is testosterone. The dominate female sex hormones are estrogen and progesterone. Sex hormones are present in both males and females but in different amounts. Hormones are chemical messengers produced by endocrine glands and the brain. Endocrine glands are located throughout the body, respond to specific signals that may increase or decrease hormone secretion.

Estrogen has a bimodal effect on the hypothalamus with both inhibitory and stimulatory influences on GnRH secretion. The stimulatory effect of estrogen is seen at the end of the follicular phase where estrogen triggers the preovulatory GnRH surge. The ability of estrogen to induce a surge declines with age in female rodents and women. This appears to be due in large part to a decrease in estrogen induction of GnRH neurons, particularly in rodents. The inhibitory effect of estrogen on GnRH secretion and GnRH gene expression has been show in in in vivo studies indicating that estrogen inhibits GnRH pulse amplitude in the early follicular and luteal phase of the

There are two specific glands that are needed for puberty, the hypothalamus and the pituitary gland. Both glands are located in the brain. The hypothalamus is responsible for many body functions including hunger, thirst and body temperature. The pituitary gland is a tiny organ that is directly attached to the hypothalamus. The glands work in tandem. The hypothalamus sends signals to the pituitary gland. When the pituitary gland receives a signal it reacts by making hormones that controls many bodily functions including puberty. Puberty begins when the hypothalamus releases the gonadotropin-releasing hormone. This special hormone signals the pituitary gland to release two additional hormones. These are the luteinizing hormone(LH) and the follicle-stimulating

Leuprolide acetate is a synthetic nonapeptide and analogue of naturally occurring luteinizing hormone releasing hormone (LHRH). It possesses greater biological potency than the natural hormone, which when introduced into the systemic circulation induces the release of luteinizing (LH) and follicle stimulating hormone (FSH) from the anterior pituitary (Schally et al., 1971). It is the blood-borne messenger between the hypothalamus and the anterior pituitary, which controls reproductive function. LHRH is a decapeptide hormone (pGlu-His-Trp-Ser-Tyr-GlyLeu-Arg-Pro-Gly-NH,), which is synthesized and stored in the hypothalamus in neurons which project to the median eminence. LHRH is released in periodic bursts into the hypophyseal portal circulation, where it induces the release of gonadotropins, luteinizing hormone (LH) and follicle stimulating hormone (FSH) into the systemic circulation. These factors then produce a trophic and steroidogenic effect upon the gonadal tissues (Rippel et al., 1974; Johnson et al., 1976).

Postnatal differentiation of human Leydig cells involves a variety of cellular cascades resulting in mature Leydig cells. When the ‘second wave’ occurs after 2-3 months of birth there is a gradual increase in testosterone levels, the neonatal cell population during this time frame is a mix of mature well-developed Leydig cells and smaller ones (52). These cells possess well-developed steroidogenic machinery expressing both the LH receptor and key steroidogenic enzymes such as 3βHSD, P450scc, P450c17 required for androgen synthesis (53). The neonatal androgen surge is believed to play a role in imprinting various cell types in the prostate, hypothalamus, genetalia and kidney, in such a way they respond appropriately to androgen stimulation during adulthood (54). The Leydig cells then regress and testis remain dormant until puberty (55).

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