The different in males and females, they are

The hypothalamic pituitary gonadal (HPG)
axis is an important structure whose main role is to maintain the male and
female reproductive system. The pituitary gonadal relationship was first suggested
in 1910. In their experiment, Crowe et al., showed that partial
pituitary ablation resulted in atrophy of the genital organs in adult dogs, and
a persistence of infantilism and sexual inadequacy in puppies (Crowe,
1910).  

Although the steroids produced in the
gonads, as an effect of the hormones released by the hypothalamus and the
pituitary are different in males and females, they are both important in
gametogenesis, stimulating bone and muscle growth and maintaining male and
female secondary characteristics respectively. In the following, similarities
and differences in how hormones secreted by the hypothalamic-pituitary-gonadal
axis affect males and females will be highlighted.  

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Similarities in the HPG axis in males and females

Gonadotropin releasing hormone (GnRH) is synthesized
and released by the hypothalamus. It is a decapeptide, released into the
hypophyseal portal circulation via endocrine neurons to act on the anterior pituitary
gland (Stamatiades
and Kaiser, 2017). This is turn leads to production of
follicle stimulating hormone (FSH) and luteinizing hormone (LH).  The HPG axis in the mid-term fetus is inactive
due to the negative feedback produced by the placental hormones. At birth, as
oestrogen levels produced by the placenta decrease, FSH and LH levels increase
and are at their peak during the first 1 – 3 months of life with levels
comparable to the time of puberty. This period is referred to as mini-puberty
and aids in gonadal activation in both sexes (Kurto?lu
and Ba?tu?, 2014). At the age of 6 months, gonadotropin
levels are noted to decrease and the axis remains quiescent until it is then
re-activated at the time of puberty, which is the developmental time in which
an organism achieves its reproductive capacity and it is at this time that GnRH
secretion increases (Herbison,
2016).

 

Figure 1. Periods of HPG axis activity (Kuiri-Hänninen,
Sankilampi and Dunkel, 2014)

Studies have shown the importance of the
pulsatile mechanism of GnRH secretion in maintaining FSH and LH production (Belchetz et al., 1978)(WILDT et al., 1981) and this mode of secretion is present in
both males and females to ultimately produce sex steroids. FSH is
preferentially stimulated at low GnRH pulse frequencies, whereas LH is
preferentially stimulated at high GnRH pulse frequencies (Ciccone
and Kaiser, 2009). Bursts occur every 1-2 hours and with
this knowledge, GnRH agonists have been developed to inhibit its effect and are
used in specific clinical situations in which reduction or abolition
of gonadotropin secretion is beneficial. Such situations include
contraception (in both male and female), and in the management of
endometriosis, precocious puberty, and sex hormone dependent cancers (‘Pulsatile
control of reproduction.’, 1984).

FSH and LH act on the gonads to produce
sex steroids. Different sex hormones are produced in the males and females
which have different end functions. In both males and females however, there is
regulatory feedback effects by the sex steroids at the pituitary and hypothalamic
levels. This is important for the proper regulation, control and function of
the axis (Kaprara
and Huhtaniemi, 2017).

 

 

 

 

 

 

 

 

 

 

 

Figure 2. Summary of the HPG axis in males and females

In 2003, kisspeptins were identified as
important proteins in the regulation of the HPG axis and in initiating puberty.
Mutations in the receptor gene GPR54 led to hypogonadotrophic hypogonadism (De Roux et al., 2003)(Seminara et al., 2003) while an activating mutation was
suggested to be the cause of precocious puberty (Teles et al., 2008). Rat and monkey studies demonstrated the
different levels of gene expression at different stages of the reproductive life
with levels minimally during the prepubertal stage, which further increase and
are at their maximum during puberty, causing an increase in the level of both
GnRH and LH which are associated with the initiation of puberty (Navarro et al., 2004)(Shahab et al., 2005)(Ebling,
2005). Other proteins apart from kisspeptins
including neurokinin B have been recently studied as to what their role is in
the initiation of puberty, however further in-depth detail is needed to
describe the exact mechanism that re-starts the HPG axis during the juvenile
years.

 

Differences in the HPG axis in males and females

While mini-puberty is seen in both males
and females with a decline in gonadotrophins in both sexes after 6 months, FSH
levels remain high in females until the age of 3 – 4 years of life. A gender
difference in gonadotrophins is also observed in the female fetus during the
first half of pregnancy, in whom serum FSH and LH levels are higher than male
fetuses (Kaplan and
Grumbach, 1976).

FSH and LH act on the gonads; the testes
in males, ovaries in females. The testes contain Leydig cells which produce
testosterone under the effect of LH. Spermatogenesis occurs in the Sertoli
cells under the effect of FSH. In females, FSH is responsible for oocyte
maturation and oestrogen production from the granulosa cells of the ovarian
follicle, while LH induces ovulation and is responsible for androgen production
in the theca cells, needed for oestrogen synthesis. In females, FSH and LH
levels vary according to the ovarian cycle with FSH mostly prominent in the
follicular phase and LH predominant in the luteal phase. In return, oestrogen
is the main hormone responsible for the follicular phase and progesterone the
main hormone produced by the corpus luteum in the luteal phase (Fauser and
van Heusden, 1997). This is in response to the varied pulse
frequency in females as opposed to the constant pulse frequency of GnRH
secretion present in males (Marshall
and Griffin, 1993). With every cycle which is approximately 30
days long, one oocyte is released from the ovarian follicles, whereas in males
thousands of sperm are produced by the Sertoli cells every day. This also
implies that females demonstrate episodic fertility periods, which coincide
with ovulation, whereas males have continual fertile potential.

Figure 3. Hormones in the ovarian cycle

Puberty typically occurs 1-2 years earlier
in females than in males (Fechner,
2002), with high levels of FSH and LH observed
at an earlier age in girls in serum levels studied in 1978 (Apter,
Pakarinen and Vihko, 1978). Recent studies have aimed to demonstrate
a reason for this with Kauffman et al., demonstrating that gonadectomy
performed during the peripubertal period stimulated Kiss 1 and Neurokinin B
expression in the hypothalamus with a secondary increase in gonadotropin
secretion in females but not in male mice and hence suggested that the neuronal
circuits activating the peripubertal reproductive axis are controlled in a
sex-specific manner with neuronal activity in females affected by gonadal
hormones as opposed to a different mechanism in males (Kauffman et al., 2009). More studies on what these mechanisms
are and what causes the initiation of puberty are needed.

Aging seems to affect the HPG axis in
females, but no so much in males. Menopause marks the end of the reproductive
life cycle in females. As this time approaches in a woman’s life, GnRH pulse
frequency decreases with a steady decrease in estradiol and progesterone
levels. In contrast, LH and FSH levels increase since negative feedback by sex
steroids on the anterior pituitary is reduced (Hoyt and
Falconi, 2015).

Similarities

Differences

GnRH released by hypothalamus in both males and
females

FSH in males declines at 6 months of life, whereas
in females it remains high until 3-4 years of age

FSH and LH release by anterior pituitary gland in
both males and females

FSH and LH levels are higher in female fetuses than
in male fetuses in the first half of life in utero

Mini-Puberty occurs in both sexes during the first 3
months of life. HPG axis then remains quiescent until puberty

Different gonads in males and females: Testes in
males, Ovaries in females

GnRH released in a pulsatile manner to maintain FSH
and LH release

Different sex steroids produced by gonads:
testosterone in males, oestrogen and progesterone in females

Negative and Positive feedback exerted to control
the HPG axis

Cyclical pulse frequency in females, constant in
males resulting in cyclical FSH and LH levels in females, constant levels in
males

Kisspeptins identified as important proteins in the
regulation of the HPG axis and in initiating puberty

One oocyte per ovarian cycle in female (average
cycle length: 30 days), thousands of sperms produced every day in males

 

Puberty occurs 1-2 years earlier in females than in
males

 

Aging affects the HPG axis in females, but not in
males

Table 1. Summary of similarities and differences in
the male and female HPG axis

The hypothalamic pituitary gonadal (HPG)
axis is an important structure whose main role is to maintain the male and
female reproductive system. The pituitary gonadal relationship was first suggested
in 1910. In their experiment, Crowe et al., showed that partial
pituitary ablation resulted in atrophy of the genital organs in adult dogs, and
a persistence of infantilism and sexual inadequacy in puppies (Crowe,
1910).  

Although the steroids produced in the
gonads, as an effect of the hormones released by the hypothalamus and the
pituitary are different in males and females, they are both important in
gametogenesis, stimulating bone and muscle growth and maintaining male and
female secondary characteristics respectively. In the following, similarities
and differences in how hormones secreted by the hypothalamic-pituitary-gonadal
axis affect males and females will be highlighted.  

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For You For Only $13.90/page!


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Similarities in the HPG axis in males and females

Gonadotropin releasing hormone (GnRH) is synthesized
and released by the hypothalamus. It is a decapeptide, released into the
hypophyseal portal circulation via endocrine neurons to act on the anterior pituitary
gland (Stamatiades
and Kaiser, 2017). This is turn leads to production of
follicle stimulating hormone (FSH) and luteinizing hormone (LH).  The HPG axis in the mid-term fetus is inactive
due to the negative feedback produced by the placental hormones. At birth, as
oestrogen levels produced by the placenta decrease, FSH and LH levels increase
and are at their peak during the first 1 – 3 months of life with levels
comparable to the time of puberty. This period is referred to as mini-puberty
and aids in gonadal activation in both sexes (Kurto?lu
and Ba?tu?, 2014). At the age of 6 months, gonadotropin
levels are noted to decrease and the axis remains quiescent until it is then
re-activated at the time of puberty, which is the developmental time in which
an organism achieves its reproductive capacity and it is at this time that GnRH
secretion increases (Herbison,
2016).

 

Figure 1. Periods of HPG axis activity (Kuiri-Hänninen,
Sankilampi and Dunkel, 2014)

Studies have shown the importance of the
pulsatile mechanism of GnRH secretion in maintaining FSH and LH production (Belchetz et al., 1978)(WILDT et al., 1981) and this mode of secretion is present in
both males and females to ultimately produce sex steroids. FSH is
preferentially stimulated at low GnRH pulse frequencies, whereas LH is
preferentially stimulated at high GnRH pulse frequencies (Ciccone
and Kaiser, 2009). Bursts occur every 1-2 hours and with
this knowledge, GnRH agonists have been developed to inhibit its effect and are
used in specific clinical situations in which reduction or abolition
of gonadotropin secretion is beneficial. Such situations include
contraception (in both male and female), and in the management of
endometriosis, precocious puberty, and sex hormone dependent cancers (‘Pulsatile
control of reproduction.’, 1984).

FSH and LH act on the gonads to produce
sex steroids. Different sex hormones are produced in the males and females
which have different end functions. In both males and females however, there is
regulatory feedback effects by the sex steroids at the pituitary and hypothalamic
levels. This is important for the proper regulation, control and function of
the axis (Kaprara
and Huhtaniemi, 2017).

 

 

 

 

 

 

 

 

 

 

 

Figure 2. Summary of the HPG axis in males and females

In 2003, kisspeptins were identified as
important proteins in the regulation of the HPG axis and in initiating puberty.
Mutations in the receptor gene GPR54 led to hypogonadotrophic hypogonadism (De Roux et al., 2003)(Seminara et al., 2003) while an activating mutation was
suggested to be the cause of precocious puberty (Teles et al., 2008). Rat and monkey studies demonstrated the
different levels of gene expression at different stages of the reproductive life
with levels minimally during the prepubertal stage, which further increase and
are at their maximum during puberty, causing an increase in the level of both
GnRH and LH which are associated with the initiation of puberty (Navarro et al., 2004)(Shahab et al., 2005)(Ebling,
2005). Other proteins apart from kisspeptins
including neurokinin B have been recently studied as to what their role is in
the initiation of puberty, however further in-depth detail is needed to
describe the exact mechanism that re-starts the HPG axis during the juvenile
years.

 

Differences in the HPG axis in males and females

While mini-puberty is seen in both males
and females with a decline in gonadotrophins in both sexes after 6 months, FSH
levels remain high in females until the age of 3 – 4 years of life. A gender
difference in gonadotrophins is also observed in the female fetus during the
first half of pregnancy, in whom serum FSH and LH levels are higher than male
fetuses (Kaplan and
Grumbach, 1976).

FSH and LH act on the gonads; the testes
in males, ovaries in females. The testes contain Leydig cells which produce
testosterone under the effect of LH. Spermatogenesis occurs in the Sertoli
cells under the effect of FSH. In females, FSH is responsible for oocyte
maturation and oestrogen production from the granulosa cells of the ovarian
follicle, while LH induces ovulation and is responsible for androgen production
in the theca cells, needed for oestrogen synthesis. In females, FSH and LH
levels vary according to the ovarian cycle with FSH mostly prominent in the
follicular phase and LH predominant in the luteal phase. In return, oestrogen
is the main hormone responsible for the follicular phase and progesterone the
main hormone produced by the corpus luteum in the luteal phase (Fauser and
van Heusden, 1997). This is in response to the varied pulse
frequency in females as opposed to the constant pulse frequency of GnRH
secretion present in males (Marshall
and Griffin, 1993). With every cycle which is approximately 30
days long, one oocyte is released from the ovarian follicles, whereas in males
thousands of sperm are produced by the Sertoli cells every day. This also
implies that females demonstrate episodic fertility periods, which coincide
with ovulation, whereas males have continual fertile potential.

Figure 3. Hormones in the ovarian cycle

Puberty typically occurs 1-2 years earlier
in females than in males (Fechner,
2002), with high levels of FSH and LH observed
at an earlier age in girls in serum levels studied in 1978 (Apter,
Pakarinen and Vihko, 1978). Recent studies have aimed to demonstrate
a reason for this with Kauffman et al., demonstrating that gonadectomy
performed during the peripubertal period stimulated Kiss 1 and Neurokinin B
expression in the hypothalamus with a secondary increase in gonadotropin
secretion in females but not in male mice and hence suggested that the neuronal
circuits activating the peripubertal reproductive axis are controlled in a
sex-specific manner with neuronal activity in females affected by gonadal
hormones as opposed to a different mechanism in males (Kauffman et al., 2009). More studies on what these mechanisms
are and what causes the initiation of puberty are needed.

Aging seems to affect the HPG axis in
females, but no so much in males. Menopause marks the end of the reproductive
life cycle in females. As this time approaches in a woman’s life, GnRH pulse
frequency decreases with a steady decrease in estradiol and progesterone
levels. In contrast, LH and FSH levels increase since negative feedback by sex
steroids on the anterior pituitary is reduced (Hoyt and
Falconi, 2015).

Similarities

Differences

GnRH released by hypothalamus in both males and
females

FSH in males declines at 6 months of life, whereas
in females it remains high until 3-4 years of age

FSH and LH release by anterior pituitary gland in
both males and females

FSH and LH levels are higher in female fetuses than
in male fetuses in the first half of life in utero

Mini-Puberty occurs in both sexes during the first 3
months of life. HPG axis then remains quiescent until puberty

Different gonads in males and females: Testes in
males, Ovaries in females

GnRH released in a pulsatile manner to maintain FSH
and LH release

Different sex steroids produced by gonads:
testosterone in males, oestrogen and progesterone in females

Negative and Positive feedback exerted to control
the HPG axis

Cyclical pulse frequency in females, constant in
males resulting in cyclical FSH and LH levels in females, constant levels in
males

Kisspeptins identified as important proteins in the
regulation of the HPG axis and in initiating puberty

One oocyte per ovarian cycle in female (average
cycle length: 30 days), thousands of sperms produced every day in males

 

Puberty occurs 1-2 years earlier in females than in
males

 

Aging affects the HPG axis in females, but not in
males

Table 1. Summary of similarities and differences in
the male and female HPG axis

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