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Science of reproduction > Puberty > Flashcards

Puberty Flashcards

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1
Q

What is puberty

A

-Complex developmental event
-Continuum of changes leading to somatic and sexual maturation
-Profound physiological, psychological and physical changes

Reproductive perspective: goal to produce mature gametes:
Testes — spermatozoa
Ovaries —-oocyte

Breast development in females, and increased testicular volume in males

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2
Q

Briefly describe the two endocrine events of puberty

A

the endocrine events are independently regulated

  • Adrenarche involves the release of adrenal androgens that allow for the growth of axillary hair and increase height
  • Gonadarche activates the HPG axis allows for the release of LH and FSH, that enable steroid synthesis and allow for the development of secondary sexual characteristics

FSH in males: growth of the testis + steroid synthesis
FSH in females: steroid synthesis+ folliculogenesis

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3
Q

What is adrenarche?

A

Adrenarche is the first endocrine event to occur, it starts to occur between the ages of 6&8 and is characterised by (re-)instigation of adrenal androgen secretion Dehydro-epiandrosterone (DHEA) and
Dehydro-epiandrosterone sulphate (DHEA-S).

These are released form the zona retiuclaris as a result of the inherent maturation and remodelling the of cellular compartments of the adrenal cortex.

There is no change in cortisol/other adrenal hormones - not a global activation of HPA axis

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4
Q

Describe adrenal remodelling during development

A

In the foetus, the foetal zone of the adrenal gland produces DHEA&DHEAS.
In the neonate, there is involution of the foetal zone, and thus a reduction in DHEA& DHEAS secretion.
In the infant, the zona glomerulosa and the zona fasiculata develop but there is no DHEA/DHEAS secretion
At 3 years focal islands develop (patches of the zona reticularis start to expand and form a layer of the zona reticularis), there is no DHEA/DHEAS secretion
At 6 years, a functional zona reticularis develops that secretes DHEA and DHEAS
At 12 to 13 years, the zona reticularis expands and secretes DHEA and DHEAS

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5
Q

How is DHEA/S synthesised?

A

Cholestrol
|
pregneolone
|
17a hydroxypregnenalone
|
DHEA
|
DHEA-sulfate

DHEA is made by the conversion of cholesterol into pregnenalone into 17a hydroxypregnenalone and consequently DHEA and DHEAS.

There is increased expression of CYP11A (responsible for the conversion of cholesterol into pregnenalone) and CYP17 & 17a-hydroxylase (converts pregnenalone into 17-a hydroxypreganalone) in the cortisol and DHEA producing cells (ZF&ZR)

CYP17 and 17,20 lyase and cytochrome b3 are highly expressed in DHEA secreting cells (ZF&ZR) , these allow for the conversion of 17a-hydroxypregnalone into DHEA or potentially into glucocorticoids via 3B HSD (expressed in low DHEA(S) secreting cells

DHEA is converted into DHEAS by SULT2A1, which is highly expressed in DHEA secreting cells (ZR)

check diagram on slide 11

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6
Q

How is DHEA/S made?

A

Cholestrol
|
pregneolone
|
17a hydroxypregnenalone
|
DHEA
|
DHEA-sulfate

DHEA is made by the conversion of cholesterol into pregnenalone into 17a hydroxypregnenalone and consequently DHEA and DHEAS.

There is increased expression of CYP11A (responsible for the conversion of cholesterol into pregnenalone) and CYP17 & 17a-hydroxylase (converts pregnenalone into 17-a hydroxypreganalone) in the cortisol and DHEA producing cells (ZF&ZR)

CYP17 and 17,20 lyase and cytochrome b3 are highly expressed in DHEA secreting cells (ZR) , these allow for the conversion of 17a-hydroxypregnalone into DHEA or potentially into glucocorticoids via 3B HSD (expressed in low DHEA(S) secreting cells (ZG&ZF)

DHEA is converted into DHEAS by SULT2A1, which is highly expressed in DHEA secreting cells (ZR)

Zona glomerulosa (ZG)
Zona fasiculata (ZF)
Zona reticularis (ZR)

check diagram on slide 11

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7
Q

Describe the function of DHEA

A

It is involved in the metabolism within peripheral tissue. Particularly the production of DHT which drives the maturation of hair follicles required for the growth of pubic and auxiliary hair.

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8
Q

What are the potential candidates for triggering adrenarche?

A
  1. ACTH?
    Dexamethasone suppresses adrenal androgen production
    -Children with ACTH receptor mutations fail to undergo adrenarche.
    -But, no change in ACTH/cortisol during adrenarche
    ACTH eventually ruled out as a factor in driving adrenarche
  2. POMC?
    (Pro-opiomelanocortin - 241AA sequence that undergoes cleavage into multiple peptides)

Proximal 18 AA region that positively regulated adrenal androgen production.

In vitro studies did not substantiate this

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9
Q

What are the potential candidates for triggering adrenarche?

A
  1. ACTH?
    Dexamethasone suppresses adrenal androgen production
    -Children with ACTH receptor mutations fail to undergo adrenarche.
    -But, no change in ACTH/cortisol during adrenarche
    ACTH eventually ruled out as a factor in driving adrenarche
  2. POMC?
    (Pro-opiomelanocortin - 241AA sequence that undergoes cleavage into multiple peptides)
    -Proximal 18 AA region that positively regulated adrenal androgen production.
    -In vitro studies did not substantiate this.
  3. POMC-related peptides?
    b-lipotrophin and b-endorphin plasma levels correlate with increased DHEA/S at adrenarche.
  4. Other factors ruled out include prolactin, IGF-1 and insulin

No conclusive mechanism for control ofadrenarche.

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10
Q

What is Gonadarche?

A

(Re-)Activation of HPG axis.
Several years after adrenarche (typically ~11 yrs of age).
Driven by hypothalamic GnRH & pituitary gonadotrophins (LH/FSH)

Puberty depends on reactivation of GnRH release

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11
Q

Describe GnRH secretion

A

GnRH is synthesised & secreted
↓
Synthesis and secretion of pituitary gonadotrophins (LH & FSH)
↓
Gonadal steroid production
↓
Negatively/positively feedback onto hypothalamus-pituitary to regulate GnRH and LH/FSH production

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12
Q

When is the HPG axis switched on? and when is it switched off?

A

16th gestational week activation of HPG axis.
Pulsatile GnRH secretion in foetus and 1-2 years postnatal increased.
Neurones ‘restrained’ during postnatal period  10 years or more
At puberty a gradual rise in pulsatile release- around 1 year before breast budding observed. “Nocturnal rise in GnRH (LH)”

*Switched off before birth due to placental hormonal function
After birth the HPG axis is switched on for the first 1 to 2 years
Then it is turned off and restrained
Then it reactivates at puberty. -

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13
Q

Define consonance and define the tanner stages of puberty

A

Consonance – smooth ordered progression of stages. There is variation in the time in each stage and time taken for each stage to progress.

The tanner stages categorise puberty for girls and boys through a criteria including measuring breast development, pubic hair development and genital development.

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14
Q

List some of the risks for precocious (early puberty)

A
  • cardiovascular disease
    • metabolic disease
    • obesity
    • diabetes
    • disordered behaviour
    • decreased adult height
    • decreased life expectancy
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15
Q

What controls the onset of puberty?

A

Dialogue between our individual genetics and environmental factors
All impinge at different points of the HPG axis

A number of theories have been put forward:
Inherent maturation of CNS
Body fat/nutrition – Leptin and Ghrelin?
Hypothalamic hormones - Kisspeptin, other factors?
Latest theories - Epigenetics

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16
Q

What is the link between energy homeostasis & reproduction

A

Secular trend to earlier age at menarche in girls from W. Europe & USA. Average age of menarche onset (UK) is 12.5yrs

This suggests that an increase in availability of nutrition and food may allow for an earlier onset of puberty

  • Extremes of energy excess (body fat mass) impact the timing of puberty in both sexes - particularly females
  • Under- and over-nutrition in foetal and/or neonates alters the timing of puberty in rodents and humans
  • Morbid obesity (females) can cause precocious puberty
  • Frisch et al.: “critical fat mass” hypothesis
    Threshold % fat/body weight is required to attain (17%) and maintain female reproductive ability (22%)

This body weight makes sense in an evolutionary context – sufficient body weight hence energy needed to nuture a child

-Cross talk between metabolic status and puberty onset/maintenance of reproduction

17
Q

How does nutrition affect puberty?

A

Gut secretion and adipose secretions module the HPG axis
A Hyperphagic, Hyperglycaemic and insulin resistant mouse was found to be Infertile and Leptin deficient

1994: leptin gene cloned
Expressed in adipocytes- WAT
Sensor of energy sufficiency
Satiety factor - tells brain you’re full
Stimulates energy expenditure
Circulating levels directly proportional to amount of body fat

Influence on reproductive system
ob/ob mice & humans - hypogonadotrophic hypogonadism
Delayed/absent puberty
Can be reversed with leptin injection
Some leptin-deficient patients have normal menses/LH/oestradial levels- unknown why.

18
Q

Does leptin trigger puberty?

A

Sexual dimorphism:
- Females- rise ~ 2 years prior to puberty (increased GnRH pulsatility)
- Males- no rise
Obesity increases leptin and earlier puberty occurs

KO leptin in rodents and humans- delayed/absent puberty

BUT, leptin administration can not stimulate early puberty

No leptin receptors on GnRH neurons

Threshold of leptin required to be reached for puberty but not a driver of puberty itself.

Leptin has a permissive role on puberty onset, not the ‘driver’

19
Q

Describe the role of Gut peptides: ghrelin in triggering puberty

A

-Ghrelin senses the fasted state, to stimulate feeding and fat deposition.
-A bolus of ghrelin stimulates the GH/IGF axis Via GHSR.
-In ‘starvation’ (high ghrelin) decreased activity of the HPG axis.
-Ghrelin decreases as puberty proceeds.

Ghrelin can decrease hypothalamic kiss1 expression in rat (Forbes et al., 2009).

Subset of kiss1 neurons in selective hypothalamic nuclei that express GHSR and respond to Ghrelin.

Oestradiol can also increase GHSR expression and response to Ghrelin in kiss1 neurons (Frazao et al., 2014).

Low levels of leptin and high levels ghrelin  decreased LH.

20
Q

What are the current theories on the trigger of puberty

A
  1. Hypothalamic hormones: kisspeptin
    Co-expression of GnRH mRNA with Kiss1R mRNA in rats from the medial preoptic area.

KiSS-1/GPR54 are expressed in the AVPV
(Anteroventral periventricular nucleus) and the arcutate nucleus)

study– investigated mRNA expression of Kiss and GPR54 in the hypothalamus of juvenile and pubertal monkeys
result: Significant difference in kisspeptin receptor activation but the receptor level didn’t change.

Activation of puberty is more downstream kisspeptin activation then the receptor

21
Q

what was the effect of of continuous kisspeptin infusion on LH release in juvenile rhesus monkeys

A

Inittial spike of LH until complete shutdown of the HOG axis

22
Q

what was the effect of of pulsatile kisspeptin infusion on LH release in juvenile rhesus monkeys

A

2 pulses of GnRH, followed by pulsatile Kisspeptin secretion
Pulsatility is also necessary for kisspepetin secretion

23
Q

What is the role of kisspeptin based on studies

A

Original observations in GPR54 null mice / humans (mutations):
Abnormal development of GnRH neurones  hypogonadism

Failure to enter puberty

KO mice for GPR54 or kisspeptin  hypothalamic hypogonadism

Mutations in humans- hypothalamic hypogonadism

Activating mutations of GPR54  precocious puberty

Phenotype (mice) –
Male: small testes and epididymis, delayed spermatogenesis infertility;
Female: small oviducts, folliculogenesis-no progression to ovulation, no oestrous cycles, infertility

24
Q

What are the effects of starvation on the expression of Kisspeptin in the hypothalamus ?

A

Indirect and direct mechanisms of Leptin action in hypothalamus on HPG axis

Reduced leptin in starvation, decreased GnRH secretion
Leptin directly excites Kiss1 neurones in ARC
Leptin deficiency »↓Kiss 1 mRNA in ARC

study: Effects of starvation on the expression of Kisspeptin in the hypothalamus of pubertal and adult mice

Results: Pubertal mice: In a fasted state, reduction in kisspeptin positive cell bodies

In adult mice: no significant difference of kisspeptin positive cell bodies between a fed and fasted state

But only 10-40% of Kiss1 neurones express LepR

25
Q

What switches on puberty?

A

an integration of central and peripheral inputs determined both by genetics and environment/nutrition

check diagram on last slide

Science of reproduction (11 decks)

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