THE PHYSIOLOGY OF GROWTH AND

DEVELOPMENT
Diah Ayu Aguspa Dita, S.Kep., Ns., M.Biomed
Department of Medical Physiology
Faculty of Medicine and Health Sciences
Universitas Bengkulu
LEARNING
OUTCOMES
• Upon completion of this lecture, students are capable
• Comprehend the concepts of growth and development;
• Comprehend the important role of hormones in the progression of growth
and development; and
• Comprehend the physiological aspects of puberty.
BASIC
CONSEPTS
GROWTH
Alterations in volume, quantity,
magnitude, or proportions at the
cellular, organ, or individual level that
are quantifiable through weight, length,
bone development, and metabolic
equilibrium  The physical dimension
DEVELOPMENT
The capacity to develop and organize
more intricate anatomical structures
and physiological processes in a
systematic manner has been enhanced
 The process of organ or
individual function maturation
THE PHASES OF GROWTH AND
DEVELOPMENT
PRENATAL POSTNATAL
(Antenatal development) (Human development)
The process encompasses the period The process of growth and change that
from the formation of an embryo, takes place between birth and maturity
through the development of a fetus, to
birth (or parturition)
PRENATAL DEVELOPMENT
Average fetal growth pattern during gestation
Age of fetus Crown to Weight
• Germinal stage (the pre-embryonic stage) (in weeks) lump (in
length (in
pounds)
• Embryonic stage inches)

• Fetal Stage 5–8 0.3 – 1.0 0.01 – 0.03

13 – 16 3.5 – 5.5 0.12 – 0.43

21 – 24 7.9 – 9.1 1.06 – 1.81

29 – 32 11.0 – 11.8 3.10 - 4.60

37 - 40 13.8 – 14.2 6.60 – 7.50

PRENATAL DEVELOPMENT
• Germinal stage (the pre-embryonic stage)
• The first two weeks of development
• Period of cell division and initial differentiation (cell maturation)

• Embryonic stage (the pre-embryonic stage)

• Period of organogenesis
• Lasts from the third to the eighth week of development

• Fetal stage
• Characterized by the maturation of tissues and organs
• Rapid growth of the body
 5nd and 6nd Months
FETAL • Downy hairs (lanugo) cover
the body, and some head
STAGE 4nd Months hairs appear
• The skin is less transparent
• The initiation of sucking
• Eyebrows and eyelashes are
motions and breathing
3nd movements begins
clearly present
• Fetal heartbeat is heard
•Months
The young fetus • The fetus ingests and
resembles human being absorbs the
2nd Months • The head is amniotic fluid
• The embryo is little disproportionately large
more than 25 mm (1 • The ears rise to eye
inch) long level
• The process of the • The eyelids fuse
development of big shut
blood vessels • Nails begin forming
• The fetal stomach
generates fluid
• The heart initiates the
circulation of blood
FETAL
STAGE 9nd Months
• Complete fetal development
• The body and limbs become
better-rounded
8nd Months • The dull redness of the skin fades
• Surfactant is produced by the and wrinkles smooth out
lungs of the fetus
• Fat is depositing beneath the
7nd Months skin
• The development of the central • The testes begin to invade the
nervous system is progressing scrotum
FETAL
STAGE The average size and weight of the baby from two to nine months
 POSTNATAL
DEVELOPMENT Senescence
• The decline in
Maturity sex
• The process of hormones
is associated
Adolescence with a
physical,
• The phase of decrease in
emotional,
Childhood and
physical
physiologica function
• 2 years – behavioral
Infants adolescence
l and maturation
reproductiv
maturation persist
• 1st Month – 2
Neonatal years
e s
• Birth – 1st
month
 FACTORS INFLUENCING GROWTH AND
DEVELOPMENT
GENETIC BEHAVIOR
Genetic machinery  determines the intensity Quality genetic  Individuals have the ability to
and speed of division, the degree of tissue engage with their surroundings constructively, so
sensitivity to stimuli, the age of puberty and the achieving the most favorable outcomes.
cessation of bone growth

ENVIRONMENT
Bio-psycho-social aspects, maternal nutrition during pregnancy,
mechanics factors, exposure to toxins and chemicals, endocrine
disruptions, radiation exposure, susceptibility to infections,
stress levels, immune system functioning, and the occurrence
of embryo anoxia.
 Weight
The
± 3,4
chest Length
kg
tends 45-55
to be cm
rounder

Extremi Head
ti es circumfe
relativel r ence
y short New 35 cm
born
infant Head
relative
HB 17-
l y
19 g/dl
large,
the face
RR 35-
HR 120- rounder
160bpm 50x/men
it
GROWTH & DEVELOPMENT IN THE FIRST YEAR
Age Growth and development
4 weeks Head is lifted above the surface
8 weeks Reflex graps
12 weeks To make contact with an offered object

3 months To raise head

3 -5 months Smile – ma-
4 months Sitting position
5-6 months Begins to roll over
6-6,5 months Able to sit alone
6,5 – 8 months Repetitive sound (ma-ma, da-da)
9-10 months To creep/to crawl, will wave bye-bye
12 months Play with toy/ball
THE ROLE OF HORMONES IN THE PROCESSES OF GROWTH AND
DEVELOPMENT
Intrauterine
Growth
1. Genetic factors The initial stage of gestation
2. Maternal factors The end of the gestational period
HORMONE?
Growth hormone, IGF-2 (The initial stage of
gestation), IGF-1 (The end of the gestational
period), Insulin
NUTRITION?
Malnutritrition during pregnancy  BBLR
ENVIRONMENT?
Smoking  BBLR
Postnatal
Growth
• Hormone?
• Growth hormone, Insulin, Thyroid
• Hormone deficiency  Stunted growth
• Replacement  period of catch-up
growth
• Glucocorticoid excess  Stunted growth
Infancy and
childhood
• Hormone:
• Growth hormone
• Thyroid
• Insulin
• Steroid adrenal
• IGF
GROWTH
HORMONE
• Polypeptide, 191 amino acids in a single chain, MW of 22,005
• Secreted by anterior pituitary  somatotrope cells
• Peak secretion  childhood
• Targeted cells: Hepar
• Fast metabolism with T1/2  6-20 menit
• Stimulation of insulin like- growth factor type 1 (IGF-1)
GROWTH
HORMONE
• Functions:
• Growth of almost all tissues of the body that are
capable of growing
• Promotes increased sizes of the cells
• Increased mitosis, with development of greater
numbers of cells and specific differentiation of certain
types of cells such as bone growth cells and early
muscle cells
GROWTH
HORMONE
• Sekresi pulsatile
• ada sekitar 8-13 puncak dalam 24 jam
• berlangsung 90 menit
• maksimal saat tidur terutama tidur dalam gelombang lambat (III dan IV)
• Mulai terdeteksi sejak minggu ke-8 kehamilan
GROWTH
HORMONE
• GROWTH HORMONE HAS SEVERAL METABOLIC EFFECTS
• Enhances body protein, decreases fat stores and
conserves carbohydrates
• HOW?
• Increased rate of protein synthesis in most cells
of the body
• Increased mobilization of fatty acids from
adipose tissue
• Increased free fatty acids in the blood
• Increased use of fatty acids for energy
• Decreased rate of glucose utilization
throughout the body
GROWTH
HORMONE
• Growth Hormone Promotes Protein Deposition in Tissues
• Enhancement of Amino Acid Transport Through the Cell Membranes
• increases amino acid concentrations in the cells  increased protein synthesis
• This control of amino acid transport is similar to the effect of insulin in con-
trolling glucose transport through the membrane

• Enhancement of RNA Translation to Cause Protein Synthesis by the

Ribosomes
• Even when the amino acid concentrations are not increased in the cells
• GH still increases RNA translation  causing protein to be synthesized in greater
amounts by the ribosomes in the cytoplasm
GROWTH
HORMONE
• Growth Hormone Promotes Protein Deposition in Tissues
• Increased Nuclear Transcription of DNA to Form RNA
• Over more prolonged periods (24–48 hours)
• GH also stimulates transcription of DNA in the nucleus  causing formation of
increased quantities of RNA
• Promotes more protein synthesis and growth if sufficient energy, amino acids,
vitamins, and other requisites for growth are available

• Decreased Catabolism of Protein and Amino Acids.

• In addition to the increase in protein synthesis, GH decreases breakdown of cell
protein
• WHY? GH also mobilizes large quantities of free fatty acids from the adipose tissues 
used to supply most of the energy for the body’s cells, thus acting as a potent “protein
sparer.”
GROWTH
HORMONE
GH enhances almost all facets of amino acid uptake and protein
synthesis by cells, while at the same time reducing the breakdown
of proteins.
GROWTH
HORMONE
• Growth hormone enhances fat utilization for energy
• Release of fatty acids from adipose tissue  increases the concentration of fatty acids in
body fluids.
• In tissues throughout the body
• GH enhances conversion of fatty acids to acetyl coenzyme A (acetyl-coa) and its
subsequent utilization for energy
• Under the influence of GH, fat is used for energy in preference to use of carbohydrates and
proteins.
• Promote fat utilization, together with its protein anabolic effect
• Causes an increase in lean body mass
• Mobilization of fat by GH requires several hours to occur
GROWTH
HORMONE
• Growth hormone enhances fat utilization for energy
• “ketogenic” effect of excessive growth hormone
• Excessive amounts of GH
• Fat mobilization from adipose tissue
sometimes becomes so great
• Large quantities of acetoacetic acid are formed by the liver and released into
the body fluids  ketosis
• This excessive mobilization of fat from the adipose tissue also frequently causes
a fatty liver
GROWTH
HORMONE
• Growth hormone decreases carbohydrate metabolism
• Decreased glucose uptake in tissues such as skeletal muscle and fat
• Increased glucose production by the liver
• Increased insulin secretion

• How?

• Gh-induced “insulin resistance,”  attenuates insulin’s actions to stimulate uptake and

utilization of glucose in skeletal muscle and adipose tissue and to inhibit gluconeogenesis
(glucose production) by the liver
• Increased blood glucose concentration and a compensatory increase in insulin
secretion
• Gh’s effects are called diabetogenic  similar to those found in patients with type 2
GROWTH
HORMONE
• Growth hormone decreases carbohydrate metabolism
• Acromegaly who have excess GH secretion is usually lean with little visceral fat
• Patients with type 2 diabetes are frequently overweight with excessive visceral fat  insulin
resistance

• Why?
• We do not know the precise mechanism by which GH causes insulin resistance and
decreased glucose utilization by the cells

• How?
• GH-induced increases in lipolysis and blood concentrations of fatty acids likely contribute
to impairment of insulin’s actions on tissue glucose utilization
GROWTH
HORMONE
• GROWTH HORMONE STIMULATES CARTILAGE AND BONE GROWTH
• Increased deposition of protein by the chondrocytic and osteogenic cells that cause bone
growth
• Increased rate of reproduction of these cells
• A specific effect of converting chondrocytes into osteogenic cells  deposition of new
bone
GROWTH
HORMONE
• GROWTH HORMONE STIMULATES CARTILAGE AND BONE GROWTH
• Principal mechanisms of bone growth
• (1) in response to GH stimulation, the long bones grow in length at the epiphyseal
cartilages  causing deposition of new cartilage, followed by its conversion into new
bone, thus elongating the shaft and pushing the epiphyses farther and farther apart

• (2) Growth hormone strongly stimulates osteoblasts

• Osteoblasts in the bone periosteum and in some bone cavities deposit new bone on
the surfaces of older bone. Simultaneously, osteoclasts in the bone remove old
bone. When the rate of deposition is greater than that of resorption, the thickness
of the bone increases.
GROWTH HORMONE SECRETION
Stimulus: (1) starvation, especially with severe protein
deficiency excitement; (2) trauma; (3) ghrelin, a hormone
secreted by the stomach before meals; and (4) some amino
acids, including arginine
GROWTH HORMONE
REGULATION
Neurons in the arcuate and
ventromedial nuclei of the
hypothalamus are sensitive to Growth hormone
blood glucose concentration inhibitory hormone
(somatostatin)

Periventricu
lar neurons
of the
hypothala
mus
GROWTH HORMONE
REGULATION
GROWTH HORMONE
SECRETION • The normal concentration of GH in the
plasma
• Adult is between 1.6 and 3 ng/ml
• child or adolescent, it is about 6
ng/ml

• These values may increase to as high as

50 ng/ml after depletion of the body
stores of proteins or carbohydrates
during prolonged starvation
THE FACTORS INFLUENCE GROWTH HORMONE SECRETION
GROWTH HORMONE
FUNCTIONS
ABNORMALITIES OF GROWTH HORMONE SECRETION
• Panhypopituitarism
• Dwarfism
• Gigantism
• Acromegaly
PANHYPOPITUITARISM
• Decreased Secretion of All Anterior Pituitary Hormones
• Onset:
• congenital (present from birth)
• may occur suddenly or slowly at any time during life
• most often resulting from a pituitary tumor that destroys the pituitary gland

• Panhypopituitarism in the Adult

• Panhypopituitarism During Childhood and Dwarfism
PANHYPOPITUITARISM
• Panhypopituitarism in the adult
• Caused by:
• Craniopharyngiomas or chromophobe tumors  compress the pituitary gland until the
functioning anterior pituitary cells are totally or almost totally destroyed
• Thrombosis of the pituitary blood vessels  occurs when a new mother experiences
circulatory shock after the birth of her baby
• Effects?
• Hypothyroidism
• Depressed production of glucocorticoids by the adrenal glands
• Suppressed secretion of the gonadotropic hormones  sexual functions are lost
PANHYPOPITUITARISM
• Panhypopituitarism in the adult
• The picture is that of a lethargic person (from lack of thyroid hormones) who is
gaining weight (because of lack of fat mobilization by growth, adrenocorticotropic,
adrenocortical, and thyroid hormones) and has lost all sexual functions
DWARFIS
M
• Deficiency of anterior pituitary secretion (panhypopituitarism) during childhood
• All the physical parts of the body develop in appropriate proportion to one another, but the
rate of development is greatly decreased
• Does not pass through puberty
• Never secretes sufficient quantities of gonadotropic hormones to develop adult sexual
functions
• 1/3 of such dwarfs  only GH is deficient
• These persons do mature sexually and occasionally reproduce
DWARFIS
M
• Defisiensi GH saja: dapat sembuh sempurna bila diobati sejak dini
• Defisiensi GH pada masa dewasa setelah pertumbuhan selesai
• Mengalami penurunan kekuatan otot (protein otot berkurang)
• Penurunan kepadatan tulang (penurunan aktivitas osteoblast selama
remodeling tulang yang berlangsung terus menerus)
DWARFIS
M
GYGANTI
SM
• Hypersecretion of growth hormone  All body tissues grow rapidly, including the bones
• WHY?
• the acidophilic cells  GH-producing cells of the anterior pituitary gland become excessively active
• Caused by  acidophilic tumors occur in the pituitary gland
• If the condition occurs before adolescence, before the epiphyses of the long bones have become fused with
the shafts  height increasing, the person becomes a giant—up to 8 feet tall.

• CHARATERISTICS:
• Hyperglycemia
• the beta cells of the islets of Langerhans in the pancreas are prone to degenerate  diabetes
mellitus eventually develops
• panhypopituitarism develops if they remain untreated
GYGANTI
SM
ACROMEGAL
Y
• Hypersecretion of GH
• If an acidophilic tumor occurs after adolescence— after the epiphyses of the long bones have
fused with the shafts
• the person cannot grow taller
• the bones can become thicker and the soft tissues can continue to grow

• CHARACTERISTICS:
• Acral-distal portion  megaly-enlargement
• Prognathism, frontal bossing, kyphosis
• Thicker skin  acromegalic facies
• Hypertrophy in internal organs  cardiomegaly, hepatomegaly, renomegaly, splenomegaly
• Hyperglycemia and insulin
ACROMEGAL
Y
ACROMEGAL
Y
THYROID
HORMONE
• Produced by thyroid glands  T3 (triiodothyronine); T4 (tyrosine)
• Most are T4; T3 is more active
• T4 is converted to T3 via peripheral deiodinases
• The solubility in plasma is very low  binds to protein (99.9%)
• Thyroxine binding globulin (TBG)  70%
• Produced in the liver and regulated by estrogen
• The half-life of T4 is 6-7 days; T3 is 10 hours
HORMON
TIROID
THE ROLE OF THYROID HORMONE IN GROWTH AND
DEVELOPMENT
• Stimulation of cerebral development and growth
• If disturbed  mentally retarded
• Enhance the sensitivity to growth hormone
• Important for normal growth, bone maturation, and tooth development
THE ROLE OF THYROID HORMONE IN GROWTH AND
DEVELOPMENT
• THYROID HORMONE DISORDERS:
• Hypothyroidism:
• The rate of growth is greatly retarded
• Hyperthyroidism:
• excessive skeletal growth often occurs  taller at an earlier age
• the epiphyses close at an early age  duration of growth and the eventual
height of the adult actually may be shortened

• Disorders?
CRETINISM
• Extreme hypothyroidism during fetal life, infancy, or childhood
• Characterized especially by failure of body growth and by mental retardation
• WHY?
• Congenital lack of a thyroid gland (congenital cretinism)  failure of the thyroid
gland to produce thyroid hormone because of a genetic defect of the gland
• Endemic cretinism  a lack of iodine in the diet

• Skeletal growth  the soft tissues are likely to enlarge excessively  obese, stocky, and
short appearance
• The tongue becomes so large  obstructs swallowing and breathing
SOMATOMED
IN
• Polypeptide secreted by liver  affected by GH
• The molecular weight  7500
• Its concentration in the plasma closely follows the rate of GH secretion
• TYPE: IGF 1 (somatomedin C) dan IGF 2
• Children with deficiency of IGF fail to grow normally even though they may have normal
or elevated secretion of GH
• E.G. The pygmy peoples of africa  small stature
• Congenital inability to synthesize significant amounts of IGF-1
• Their plasma concentration of GH is either normal or high, diminished amounts
of IGF-1 in the plasma
INSULIN LIKE GROWTH FACTOR-1
(IGF-1)
• IGF1 secretion before birth  independent of GH
• After birth dependent on GH strong effect on growth and development
• Nutritional status, age, gonadotropins, sex hormones
• Peak concentration during puberty
• Decreasing to a low-level  senility
SEX
HORMONE
• Important during puberty  anabolic effect on protein, stimulated by androgen
• Both sex  Adrenal androgen secretion increases
• Estrogen; androgen  increase growth hormone response
• Stop growth
• Epiphysis fused with long bones (epiphyseal closure)  linear growth
ceased
INSULI
•NProvides the energy required for growth
metabolic rate
• Promotes cellular uptake of a different
selection of amino acids
• Promote bone formation
GLUCOCORTIC
•OID
Serves as inhibitory factors of growth
• MECHANISM?
• REMAIN UNCLEAR

• The secretion of cortisol is characterized by circadian dan ultradian variability

THE PHYSIOLOGY OF
PUBERTY
PUBER
•TY
Transitional period from children to adults
• Onset:
• Girls: 8-13 years old
• Boys: 9.5 – 13.5 years old
• Basic alterations:
• Neuroendocrine changes: gonadotropin, sex steroid, growth hormone
• Physical changes: linear growth, body composition, genital organ
• Late onset:
• There are no secondary sexual changes in girls over 13 years of age
• Menarche did not occur at the age of 15 years
• Boys  There was no change in testicular size at 14 years of age
PUBERTAL
•SIGNS
The reproductive organs mature and have the ability to produce gametes
• The appearance of secondary sex characteristics
• The transformation of a child's physique into an adult's body
• Psychological changes
PUBERTAL
DEVELOPMENT
PUBERTAL AXIS
DEVELOPMENT
PUBERTAL
STAGES
• Prepubertal stage
• Children aged 8-9 years
• Dormant hypothalamic-pituitary-gonadal axis, LH and sex hormones are not found in serum,
there is an increase in DHEAS
• Peripubertal stage
• 3 years before the onset of puberty  In serum during sleep there is LH whose secretion
occurs in a pulsatile manner reflecting episodes of hypothalamic GNRH release
• Early puberty stage
• Occurs as an active hypothalamic-pituitary-gonadal interaction
• Midpuberty stage
• LH becomes more pronounced even during the day and occurs at 90 - 120 minutes
intervals
• In women, monthly cycles and ovulation occur.
Gender-specific self-assessment questionnaire for children, containing both illustrations and explanatory
text, modified from a previous study.14 (Text was translated from an original Danish version

Anna R. Rasmussen et al. Pediatrics 2015;135:86-93

CHANGES IN PLASMA HORMONE CONCENTRATION DURING PUBERTY
Boys

Girls

Anna R. Rasmussen et al. Pediatrics 2015;135:86-93

ADRENARC
•HE
Increased activity of the suprarenal cortex (adrenarche)
• Increased adrenal androgen dehydroepiandrosterone (DHEAS) secretion
• Age 6-8 years  before there is an increase in LH and other sex hormones
• Signs:
• Appearance of axillary and pubic hair in women
• Appears body odor
FACTORS AFFECTING
•PUBERTY
Genetic factors
• Nutritional status (Height and weight ratio)
• Maturation of the hypothalamus
• Onset of adrenal androgenic activity
NORMAL GROWTH
CURVE
GROWTH CURVE BY
GENDER
PUBERTY BY
GENDER
PUBERTY BY
GENDER BOYS
• Activation of the hypothalamic-pituitary-axis,
proliferation of Leydig cells in the testes 
increased synthesis and secretion of testosterone
by Leydig cells
• The growth of the testicles is wider due to an
increase in the number of seminiferous tubules,
the growth of accessory sex organs such as the
prostate
• The epiphyses close when the height is maximal
• Plasma testosterone level increases, axillary, pubic
and facial hair appears, penile growth, deeper
voice, and initiation of spermatogenesis
GIRLS
• Activation of the hypothalamic-pituitary-axis
which regulates estradiol synthesis by the
ovaries
• Enlargement of the breasts and 2 years later
the menstrual cycle occurs
• The epiphyses close more quickly in women
than in men
• The appearance of pubic and axillary hair is
dependent on increased adrenal androgen
secretion
PUBERTY
DEVELOPMENT
PUBERTY
DEVELOPMENT
TYPICAL SIGNS OF PUBERTY
IN BOYS
HORMONE REGULATION DURING
PUBERTY
HORMONE REGULATION DURING
PUBERTY
• Hypothalamus:
• GnRH, Growth Hormone Releasing Hormone (GHRH), Adrenocorticotropin
(ACTH)
• Pituitary:
• Leutinizing Hormone (LH), Follicle Stimulating Hormone (FSH), Growth
Hormone (GH)
• Gonadal and adrenal steroidogenesis
• Estradiol (girls) dan testosterone (boys), Dehydroepiandrosterone (DHEA),
Insulin-like growth Factor (IGF-I), Ghrelin
HORMONE REGULATION DURING
PUBERTY
GnRH
• In the fetus, GnRH pulsatile secretion from the hypothalamus  produce sexual
differentiation
• Before puberty, pulsatile GnRH secretion is slow
• Pulsatile secretions increase during puberty  controlled by the "developmental
clock"
• GnRH in the pituitary increases the pulsatile secretion of LH and FSH
HORMONE REGULATION DURING
PUBERTY
LH and FSH
• Enters the circulation  reaches the gonads  helps the formation of gametes
and steroid hormones
• Pulsative secretion of gonadotropins  regulates the maturation of secondary
sex characteristics
• Gonadotropin secretion is lowest at the age of 3-4 years  increasing
constantly
• Once puberty is reached  FSH rises faster than LH and reaches adult levels
before LH
• Adult gonadotropin levels reach 2-5x higher than children
HORMONE REGULATION DURING
PUBERTY
Sex steroid/estradiol
• Estradiol is the active form of estrogen
• Functions:
• Linear growth
• Epiphyseal fusion and cessation of longitudinal growth
• Mediates the maximal bone mass increase
• In adults  maintain bone mass
• Enhancement of gh release
• Development of genital organs and appearance of secondary sex
characteristics
• Menarche and the cycle of estrogen secretion
HORMONE REGULATION DURING
PUBERTY
Growth Hormone
• Rapid growth during puberty
• Secretions increase 2x during puberty
• Maximal improvement is seen at Tanner stages 3-4 in females
• The elevation in estradiol during puberty  mediates the increase in growth
hormone and directly affects bone
HORMONE REGULATION DURING
PUBERTY
Ghrelin
• A peptide hormone, secreted by oxyntic cells in the stomach
• The target receptor is the GH secretagogue (GHS) receptor
• Increase in appetite during puberty
• Increases GH secretion
HORMONE REGULATION DURING
PUBERTY
IGF-1
• GH increases IGF-1 (somatomedin C) in bones
• Levels remain elevated 1-2 years after the pubertal growth spurt
• Functions:
• IGF-1 mediates chondrocyte growth in bone
• IGF-1 mediates negative feedback for GH
HORMONE REGULATION DURING
PUBERTY
THE ROLE OF LEPTIN DURING
•PUBERTY
A hormone produced by adipose cells  stimulates satiety
• the relationship between weight gain and puberty
• A critical weight must be reached  puberty can occur
• Young women who do strenuous exercise  lose weight and stop menstruating
• If the woman starts eating and gains weight  Menstruation will return or
relapse to puberty
• Obese mice that cannot produce leptin will be infertile  fertility is cured by
leptin injection
• Leptin treatment triggers precocious puberty in immature female mice
THE ROLE OF THE GONADS DURING
•PUBERTY
Prepubertal: testosterone levels remain low (< 20 ng/dL), testes significantly increase in
size due to tubular changes in the gonads
• When testosterone levels begin to rise  increase rapidly over 10 months  associated
with pubertal growth spurt
• Circulating testosterone during puberty increases >20x compared to adults (between
300-1200ng/dL)
• Spermatogenesis begins at the age of 14 years
• Secretion from the testes and the conversion of other hormones to estrogen  Estradiol
increases during puberty
THE ROLE OF THE GONADS DURING
•PUBERTY
Prepubertal ovaries  less changes in histological development
• Plasma estrogen level < 10 pg/mL before puberty
• At 10 years old:
• Estradiol levels in women increase 2x compared to men, then there is a
constant increase in estradiol during puberty
PRECOCIOUS
•PUBERTY
Early emergence of secondary sex traits without gametogenesis
• Occurs as a result of abnormal exposure:
• Males are immature by androgens or females by estrogens  precocious
pseudopuberty
• Arises from a hypothalamic lesion that interferes with the normal pathways that inhibit
GnRH secretion
THE CAUSES OF PRECOCIOUS
PUBERTY
DELAYED
PUBERTY
• Delayed:
• Menstrual cycle does not occur until the age of 17
• Testes do not develop until the age of 20
• Caused by panhypopituitarism associated with dwarfism and other endocrine disorders
• In some individuals, delayed puberty occurs even when the gonads and other endocrine
functions are normal
• In women, it is caused by severe stress and accumulation of body calories  by
melatonin
• It is an inhibitor of GnRH release
• In boys  eunuchoidism
• In girls  primary amenorrhea
EARLY PUBERTY IN OBESE
GIRL
REFERENC
•ES
Mazziotti, G., Giustina, A. Glucocorticoids and the regulation of growth hormone secretion. Nat Rev Endocrinol 9, 265–276
(2013). https://doi.org/10.1038/nrendo.2013.5
• Sapunar, Damir , Arey, Leslie B. and Rogers, Kara. "prenatal development". Encyclopedia Britannica, 30 Oct. 2022, https://
www.britannica.com/science/prenatal- development. Accessed 15 August 2023.
THANK YOU