2024 Hormones (Part 2)

OLFU MEDICINE Biochemistry | Dra. Echaves | June 7, 2021

INTRODUCTION ANTERIOR PITUITARY

The Anterior Pituitary Gland releases these hormones, so:

• TSH for your Thyroid Gland
• ACTH for Adrenal Cortex
• FSH and LH for Testes or Ovaries
• Growth Hormone (GH) for Entire body
• Prolactin (PRL) for Mammary Glands (in Mammals)
• Endorphins for Pain Receptors in the Brain

Produced in response to TRH and the

THYROID STIMULATING HORMONE hypothalamus, so this actually
(TSH) stimulates the release of T3 and T4
from the thyroid gland

Would be released from the

hypothalamus, this protein product of
proopio-melanocortin (POMC) gene is
the big precursor molecule that is
Here are some of the organs that actually have actions regulated by later on cleaved into a number of
your hormones polypeptides depending on the tissue
• Pineal Gland where they are at.
• Hypothalamus
• Pituitary Gland
• Adrenocorticotrophic Hormone
• Thyroid Gland
(ACTH) that stimulates the
• Parathyroids
• Thymus production of cortisol and has a
• Adrenals permissive effect on the production
• Pancreas of aldosterone by the adrenal
• Ovary cortex.
• Testes
• Heart
• Liptropin (LPH) - another
• Brain CORTICOTROPIN RELEASING
polypeptide produced from your
• Cells of GIT HORMONES
POMC. This may be cleaved to form
the melanocyte stimulating
hormone and endorphins.
HYPOTHALAMUS
• Melanocyte Stimulating Hormone
• Produces vasopressin (VP) and (MSH), also came from POMC (part
Oxytocin (OT), and it also produces of ACTH and LPH), stimulates the
other hormones that regulate the production of pigment melanin by
synthesis and release of hormones the melanocyte in the skin.
from the anterior pituitary
• Endorphins produce analgesic
• Vasopressin (ADH [Anti-Diuretic effect.
Hormone]) and Oxytocin (OT) are
synthesized in the Hypothalamus
and travel through nerve axons to
the posterior pituitary where they
are stored.

• VP (ADH) is released in response to

decrease in blood volume or
increased NA+ (Sodium Ion)
concentration, when this is
happening there is a stimulation of
resorption of water by the kidney
tubules.

• Oxytocin (OT) promotes the

ejection of milk from the mammary
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gland in response to suckling and
the contraction of the uterus during
childbirth

 • Stimulate the gonads to release
hormones that are involved in
LUTEINIZING HORMONES (LH) &
reproduction.
FOLLICLE STIMULATING
• The release of LH and FSH
HORMONE (FSH)
stimulated by GnRH and inhibited
by GnRH from hypothalamus.
Stimulates the release of insulin-like
growth factors (IGFs) and
antagonizes the effect of insulin on
carbohydrate and fat metabolism. The
GROWTH HORMONE (GH)
release of GH is stimulated by GnRH
and inhibited by somatostatin from
the hypothalamus.
released in response to PRH from the
hypothalamus caused by sucking of
an infant, and it stimulates the
PROLACTINE (PRL)
synthesis of milk proteins during
lactation. Dopamine from the
hypothalamus inhibits PRL release.
THYROID HORMONES
• T3 is more active metabolically than T4.
• Thyroid gland secretes some amount of T3, and majority of them are in T4 so
this T4 can then be peripherally deiodinated into your T3. (Thyroid seceretes
some amount of T3, Majority is produced by peripheral deiodination of T4 in
nonthyroidal tissues).
• During starvation, T4 is converted to reverse T3 (rT3) which is not active.
• Thyroid Hormones bind to nuclear receptors and regulate expression of
many genes necessary for growth, development and maintenance of almost
all tissues of the body.
• It stimulates oxidative metabolism and causes the basal metabolic rate to
increase.
1ST RING 2ND RING
T3 (Metabolically
1 iodide 2 iodide
Active)
Reverse T3 (rT3) 2 iodide 1 iodide
GROWTH HORMONES
• Insulin and growth hormones stimulate growth and promote protein
synthesis.
• Growth Hormone (GH) antagonizes many metabolic actions of insul,
stimulating gluconeogenesis and promoting lipolysis. This results to
alternative fuels being made available so that the muscle protein can be
preserved.
STRESS RESPONSE
• Glucocorticoid (particularly Cortisol) and Epinephrine act in concert to
supply fuels to the body so that energy can be produced to combat a
stressful situation.
• In response to ACTH, the adrenal cortex produces glucocorticoids.
It affects fuel metabolism by causing the movement of fuels from
peripheral tissues to the liver, where gluconeogenesis and glycogen
synthesis are stimulated. It induce the synthesis of phosphoenol-pyruvate
carboxykinase (PEPC), an enzyme of gluconeogenesis.
It causes lipolysis in adipose tissues and release of amino acids in muscle
protein. This results to glucose from glucocorticoid stimulation and
stored in the liver as glycogen.
• Glucocorticoids prepare the body for possible stressful situation so that fuel
stores are ready for the “alarm” reaction which is triggered by epinephrine.
• Epinephrine increases blood glucose by stimulating liver gylcogenolysis. It
stimulates lipolysis in adipose tissue and glycogen degradation in muscles.
• Overall, it makes fuel available for sympathetic response which is your “fight
or flight response”
CORTISOL
• major glucocorticoid in humans
SALT & WATER BALANCE
• Vasopressin, your Atrial Natriuretic Peptide (ANP), and Aldosterone are
involved in salt and water balance.
Renin is produced by the kidney juxtaglomerular cells in response to
decrease in blood pressure, blood volume or blood sodium
concentration.
It cleaves the angiotensinogen to angiotensin I
Angiotensin I is cleaved to Angiotensin II by the angiotensin converting
enzyme (ACE) produced in the lung.
• Angiotensins I and II, along with decreased in sodium and increased
potassium stimulates the zona glomerulosa to produce aldosterone.
• Aldosterone causes the production of proteins in the renal tubular cell. An
enzyme permease is produced that allows sodium to enter the cells from the
lumen. In general, Potassium Ion (K+) and Hydrogen Ion (H+) are lost,
Sodium Ion (Na+) is retained, and blood volume and pressure are increased.
ANGIOTENSIN CONVERTING ENZYME (ACE)
• produced in the lung
ANGIOTENSIN II
• acts directly on vascular smooth muscle cells, causing vasoconstriction,
which increases blood pressure.
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 • Progesterone inhibits the milk protein production and secretion during

pregnancy. But, at term, diminishing progesterone level so that it relieves the
REPRODUCTION inhibition on milk protein synthesis.
• So after birth with the delivery of your placenta, there is nothing more to
• Hypothalamus produces Gonadotropin Releasing Hormone (GnRH) , which prevent or inhibit your prolactin, thereby you now have milk production.
causes the anterior pituitary to release FSH and LH, which act on both ovary
and testis. PRL stimulates the synthesis of the milk proteins:
1. Casein
• FSH and LH act on the ovary by influencing the menstrual cycle. 2. Alpha-lactalbumin
Initially, FSH acts on the follicle to promote maturation of the ovum and Major protein in human milk, serves as nutrient
stimulate estradiol (E2) production and secretion. Binds to galactosyltransferase, decreasing its Km for glucose, and
Estradiol (E2) acts on the uterine endometrium, causing it to thicken and stimulating synthesis lactose (milk sugar)
vascularize in preparation for the implantation of the fertilized egg. • Suckling of the infant stimulates the secretion of both PRL and oxytocin by
A surge of LH at the midpoint of the menstrual cycle stimulates the ripe the pituitary
follicle to ovulate. • PRL – during lactation, causes milk proteins to be produced and secreted
Cleaving the residual follicle which forms the corpus luteum, which will into the alveolar lumen
secrete both progesterone and E2. • Oxytocin – contracts the myoepithelial cells surrounding the alveolar cells
causing milk ejection through the nipple
• Progesterone causes the endometrium to continue to thicken and
vascularize and increase in secretory capacity.
• In the absence of fertilization, the corpus luteum regresses due to diminished GROWTH & DIFFERENTIATION
LH levels. This will result in declining progesterone and estradiol.
• Diminishing steroid hormone support causes the cells of the endometrium RETINOIC ACID
to die, slough off in the uterine cavity and excreted (menstruation). Is involved in growth and differentiation
• Low level of E2 and progesterone causes feedback inhibition to be It maintains the epithelial tissue
relieved, the hypothalamus releases GnRH and you now again have the start It also activates genes acting like a steroid hormone
of a new menstrual cycle.
• So in the presence of fertilization, the corpus luteum is maintained initially by Retinoids are produced in the body from dietary vitamin A, Beta-carotene
the human chorionic gonadotropin (hCG) produced by the cell of the Beta-carotene is cleaved to two molecules of retinal.
developing embryo (trophoblast). 15,15’ dioxygenase cleave it into two molecules of retinal.
• Eventually, the placenta will produce hCG and progesterone. After the
corpus luteum dies it will continue to produce large amounts of • Retinal is a functional part of the visual cycle.
progesterone. And it can also be oxidized into retinoic acid which is non-reducible.
hCG and progesterone level falls. Fetal cortisol may cause decline in (Oxidation of retinal produces retinoic acid (non-reducible).
progesterone. Prostaglandin F2α (PGF2α) and oxytocin (released from • Redox reactions intervconvert retinal and retinol.
both maternal and fetal pituitaries) stimulate uterine contraction, and Retinol, the transport form is stored as retinyl esters.
infant is delivered.
• On the testis, FSH and LH stimulate leydig cells to produce and secrete
testosterone. FSH act on the sertoli cells in the seminiferous tubules to
CALCIUM METABOLISM
stimulate the synthesis of Androgen binding protein (ABP).
• ABP binds testosterone and transports it to the site of spermatogenesis,
• Calcium combines with phosphate to form the hydroxyapatite bone cement
where it is reduced to the more potent androgen, dihydrotestosterone (DHT).
• Testosterone plays a role in spermatogenesis, masculinization during the
• Free Calcium
early life and occurrence of secondary sexual characteristics.
For blood coagulation;
Activation of muscle phosphorylase; and
Secretory processes
LACTATION
• Major Regulators of Calcium Metabolism involved:
Parathyroid hormone;
1,2-DHC (125 dihydroxycholecalciferol); and
Calcitonin

• We see here the inactive breast and lactating breast. So estrogen causes the
growth of ducts and inhibits milk production.
• Progesterone promotes the growth of lobules, but still inhibits milk
production.
• During pregnancy, major hormones responsible for the differentiation of
mammary alveolar cells into secretory cells capable of producing milk are:
Prolactin (PRL)
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Glucocorticoid
Insulin

 REVIEW:
• Vitamin D from our diet needs to go:
liver to get a hydroxyl group at Carbon 25 (25-OH-D)
and it proceeds to the kidney to get a second hydroxyl group on
Carbon 1.
• So if your parathyroid gland will sense a low serum calcium level, it will
increase the release of parathyroid hormone.
• So with the parathyroid hormone, it now acts on the bone and the kidney
Its action on the kidney is to increase the formation of active Vitamin
D and
it also decreases the excretion of calcium.

• The formed Vitamin D, the Active Vitamin D, will influence the increase in
absorption of dietary calcium from the small intestine so that this will cause
an increase in serum calcium.
• On the bone, your parathyroid hormone causes the release of calcium and
phosphorous, thereby also increasing the serum levels of calcium.
• Calcitonin lowers the CA2+ levels by inhibiting the release from the bone.
• It also causes the excretion of Calcium from your kidneys (Calcitonin lowers
CA2+ levels by stimulating urinary excretion from your kidneys).

UTILIZATION OF NUTRIENTS

from the gastric antrum and the

GASTRIN duodenum stimulates gastric acid
and pepsin secretion.

from the duodenum and jejunum

stimulates contraction of the gall
CHOLECYSTOKININ (CCK) bladder and the secretion of
pancreatic enzymes.

from the duodenum and jejunum

stimulates the secretion of
SECRETIN
bicarbonates by the pancreas.

from the small bowel enhances

insulin release and inhibit secretion
GASTRIC INHIBITORY PEPTIDE (GIP)
of gastric acid.

from the pancreas relaxes smooth

VASOACTIVE INTESTINAL PEPTIDE muscles and stimulate bicarbonate
(VIP) by secretion by the pancreas.

FUEL METABOLISM

INSULIN GLUCAGON

Fed state Fasting state

Increase availability of glucose and

Stores glyocgen and triacylglycerol
fatty aids in the blood

• Glycogenesis in the liver and • Glycogenolysis in liver, but not in

muscle muscle
• TAG synthesis in the liver • Lipolysis in adipose tissue
• Conversions to very low density • Gluconeogenesis
lipoproteins (VLDL)
• Glucose transport in muscle &
adipose cells
• Protein synthesis for growth

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