Puberty Flashcards
Define Puberty
A complex developmental event
A continuum of changes leading to somatic and sexual maturation
Profound physiological, psychological and physical changes
From a reproductive perspective the goal is to produce mature gametes
Includes breast development in females and increased testicular volume in males
What are the 2 endocrine events in puberty
Adrenarche: Activation of adrenal androgens, causing the growth of pubic axillary hair+ growth in height
Gonadarche: LH/FSH is activated
Adrenarche
First endocrine process of puberty
Occurs 6-8 years
Characterised by re-instigation of adrenal androgen secretion:
DHEA and DHEA-S
Released from the zona reticularis
(we say re-instigation because adrenal androgens go down from birth to 1 year then start to increase again aged 7)- graph is U shaped for age vs DHEAS
No change in cortisol/other adrenal hormones so doesn’t fully activate HPA axis
Stages of adrenal remodelling
Foetal zone (foetus)
Involution of FZ (neonate)
Zona glomerulosa and zona fasciculata (Infant)
Focal islands of ZR (3 years)
Expansion of ZR focal islands (4-5 years)
Functional ZR developed (6 years)—– therefore DHEAS is produced again
ZR expansion (6 years)
How is DHEA/s made
Cholesterone - pregnenolone
pregnenonlone- 17 a-hydroxypregnenolone
DHEA - DHEA sulfate
Stains used for immunohistochemistry of adrenal cortex in early adrenarche
Cytochrome B5, SULT2A1, 3BHSD
These are used to highlight glomerulosa, fasciculata, reticularis
Role of DHEA S
Low DHEA-S has been associated with ageing and coronary artery stenosis
What instigates adrenarche
Dexamethasone suppresses adrenal androgen production
Children with ACTH mutations fail to undergo adrenarche
No change in cortisol/ACTH during adrenarche
POMC- proximal 18AA region that positively regulated adrenal androgen production- shown to be incorrect
However, POMC related peptides such as b-lipotrophin and b-endorphin correlate with increased DHEA/S at adrenarche
Explain Gonadarche
Is the reactivation of HPG axis
Occurs several years after adrenarche- usually 11 years
Driven by HPG axis:
GnR- Gonadotrophins (LH/FSH)- Steroidogenesis
GnRH relationship with puberty
16th gestational week activation of HPG axis
Pulsatile GnRH secretion in foetus
Neurones restrained during postnatal period and at puberty a gradual rise occurs in pulsatile release
What are the potential risks of early puberty
Cardiovascular disease Metabolic disease Obesity Diabetes Disordered behaviour Decreased adult life expectancy and height
What controls the onset of puberty
Dialogue between individual genetics and environmental factors
Theories put forward:
Inherent maturation of CNS
Body fat/nutrition- Leptin and Ghrelin. Morbid obesity in females can cause precocious puberty. Circulating leptin levels are proportional to body fat and act as a satiety factor to tell your brain you’re full. Can be reversed with leptin injections. But- some leptin deficient patients have normal menses- unknown reason
Hypothalamic hormones such as kisspeptin
Epigenetics- latest theories
Ghrelin- gut peptide
Ghrelin senses the fasting state
Stimulates feeding and fat depostion
Starvation= High ghrelin
High grelin- Decreased activity of HPG acis
Ghrelin decreases as puberty proceeds
Ghrelin decreases hypothalamic kiss1 expression in rats
Onset of puberty because of kisspeptin
produced in AVPV and Arcuate nucleus
in studies, those with kisspeptin mutations can have:
hypogonadism from abnormal development of GnRH neurones
Failure to enter puberty
hypothalamic hypogonadism
activating mutations of GPR54- precocious puberty
