Transcript Lecture 11. Role of endocrinic glands in regulation of body functions

Role of endocrinic
glands in regulation of
body functions
Pineal Gland produces
Dimethyltryptamine
 Melatonin
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Function
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The pineal gland was originally believed to be a
"vestigial remnant" of a larger organ (much as the
appendix was thought to be a vestigial digestive organ).
It was only after the 1960s that scientists discovered
that the pineal gland is responsible for the production of
melatonin, which is regulated in a circadian rhythm.
Melatonin is a derivative of the amino acid tryptophan,
which also has other functions in the Central Nervous
System. The production of melatonin by the pineal
gland is stimulated by darkness and inhibited by light.
[7] The retina detects the light, and directly signals and
entrains the suprachiasmatic nucleus (SCN). Fibers
project from the SCN to the paraventricular nuclei
(PVN), which relay the circadian signals to the spinal
cord and out via the sympathetic system to superior
cervical ganglia (SCG), and from there into the pineal
gland.
Thyroid gland produces
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Triiodothyronine (T3), the potent form of
thyroid hormone
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Thyroxine (T4), a less active form of thyroid
hormone
Calcitonin
Tetraiodothyronine (T4) or Thyroxine
-Triiodothyronine (T3)
a) helps regulate the metabolic rate of all
cells and cell growth and tissue
differentiation.
Calcitonin
a) influence the processing of calcium by bone
cells by decreasing blood calcium levels and
promoting conservation of hard bone matrix.
Parathyroid gland produces
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Parathyroid hormone (PTH)
Parathyroid Hormone (PTH)
a) an antagonist to calcitonin and acts to maintain
calcium homeostasis.
b) acts on bone: causes more bone to be dissolved,
yielding calcium and phosphate, which enters the
bloodstream.
c) acts on kidney: causes phosphate to be secreted by
the kidney cells into the urine to be excreted.
d) acts on intestinal cells: causes increased intestinal
absorption of calcium by activating vitamin D.
Thymus
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The thymus plays an important role in the
development of the immune system, being the
primary site of T cell maturation. The organ is
most active between the late stages of gestation
and early puberty, when most of the T cells an
individual will carry for their lifetime are formed.
With the onset of puberty the organ atrophies,
gradually shrinking in size and function. The
atrophy is due to the increased circulating level of
sex hormones, and chemical or physical castration
of an adult results in the thymus increasing in size
and activity.
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In the two thymic lobes, lymphocyte
precursors from the bone-marrow become
thymocytes, and subsequently mature into T
cells. Once mature, T cells emigrate from the
thymus and constitute the peripheral T cell
repertoire responsible for directing many
facets of the adaptive immune system. Loss of
the thymus at an early age through genetic
mutation or surgical removal results in severe
immunodeficiency and a high susceptibility to
infection.
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The ability of T cells to recognize foreign
antigens is mediated by the T cell receptor. The
T cell receptor undergoes genetic rearrangement
during thymocyte maturation, resulting in each
T cell bearing a unique T cell receptor, specific
to a limited set of peptide:MHC combinations.
The random nature of the genetic
rearrangement results in a requirement of
central tolerance mechanisms to remove or
inactive those T cells which bear a T cell
receptor with the ability to recognise selfpeptides.
Heart produces
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Atrial-natriuretic peptide (ANP)
ANH’s primary effects is to oppose increases
in blood volume or blood pressure;
Also antagonist to ADH and aldosterone
Stomach and intestines produce
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Cholecystokinin (CCK)
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Gastrin
Neuropeptide Y (NPY)
Secretin
Somatostatin
Liver produces
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Insulin-like growth factor (IGF)
 Angiotensinogen
 Thrombopoietin
Islets of Langerhans in the pancreas
produce
Insulin
 Glucagon
 Somatostatin
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1) Alpha cells secrete glucagons.
2) Beta cells secrete insulin and amylin
3) Delta cells secrete somatostatin.
4) F1 or PP1 cells secrete pancreatic
polypeptides.
Name of
cells
Product
% of islet
cells
Function
beta cells
Insulin and
Amylin
50-80%
lower blood sugar
15-20%
raise blood sugar
alpha cells Glucagon
delta cells
Somatostatin
3-10%
inhibit endocrine
pancreas
PP cells
Pancreatic
polypeptide
1%
inhibit exocrine
pancreas
Insulin
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Action on carbohydrate metabolism:
1. Increase permeability of cell
membrane to glucose.
2. Stimulate synthesis of glycogen.
3. Activate transformation of
carbohydrates into fats
4. Decrease development of glucose from
amino acids.
Action on fat metabolism.
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1. Decrease destruction of fat
2. Activates synthesis of fatty acids
3. Inhibit development of ketonic bodies.
Action on protein metabolism.
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1. Increase transmission of amino acids in
cells.
2. Increase synthesis of proteins.
3. Decrease destruction of amino acids.
The actions of insulin on the global
human metabolism level include:
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Control of cellular intake of certain substances,
most prominently glucose in muscle and
adipose tissue (about ⅔ of body cells).
Increase of DNA replication and protein
synthesis via control of amino acid uptake.
Modification of the activity of numerous
enzymes (allosteric effect).
Mechanism of glucose dependent
insulin release
-Glucagon
1. tends to increase blood glucose levels
2. stimulates gluconeogenesis in liver cells
(transformation of fatty acids and amino acid
into glucose).
3. increase glycogen conversion to glucose in
liver cells.
4. stimulate lipolysis in liver.
Increased secretion of glucagon is
caused by:
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Decreased plasma glucose
Increased catecholamines - norepinphrine and
epinephrine
Increased plasma amino acids (to protect from
hypoglycemia if an all protein meal consumed)
Sympathetic nervous system
Acetylcholine
Cholecystokinin
Decreased secretion of glucagon
(inhibition) is caused by:
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Somatostatin
Insulin
Function
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Glucagon helps maintain the level of glucose in the
blood by binding to glucagon receptors on
hepatocytes, causing the liver to release glucose stored in the form of glycogen - through a process
known as glycogenolysis. As these stores become
depleted, glucagon then encourages the liver to
synthesize additional glucose by gluconeogenesis.
This glucose is released into the bloodstream. Both of
these mechanisms lead to glucose release by the liver,
preventing the development of hypoglycemia.
Increased free fatty acids and ketoacids into the blood
Increased urea production
-Somatostatin
1. Regulate the other endocrine cells of the
pancreatic islets.
Somatostatin is classified as an
inhibitory hormone, whose main
actions are to:
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Inhibit the release of growth hormone (GH)
Inhibit the release of thyroid-stimulating hormone (TSH)
Suppress the release of gastrointestinal hormones
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Lowers the rate of gastric emptying, and reduces smooth muscle contractions and
blood flow within the intestine.
Suppress the release of pancreatic hormones
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Gastrin
Cholecystokinin (CCK)
Secretin
Motilin
Vasoactive intestinal peptide (VIP)
Gastric inhibitory polypeptide (GIP)
Enteroglucagon (GIP)
Inhibit the release of insulin
Inhibit the release of glucagon
Suppress the exocrine secretory action of pancreas.
Somatostatin opposes the effects of Growth Hormone-Releasing Hormone (GHRH)
Kidney produces
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Renin
Erythropoietin (EPO)
Calcitriol (the active form of vitamin D3)
Skin produces
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Vitamin D3 (calciferol)
Adipose tissue
Leptin
 Estrogens (mainly estrone)
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Testes
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Androgens (chiefly testosterone)
Testosterone
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Testosterone is a steroid hormone from the androgen
group. Testosterone is primarily secreted in the testes
of males and the ovaries of females although small
amounts are secreted by the adrenal glands. It is the
principal male sex hormone and an anabolic steroid.
In both males and females, it plays key roles in health
and well-being. Examples include enhanced libido,
energy, immune function, and protection against
osteoporosis. On average, the adult male body
produces about twenty to thirty times the amount of
testosterone that an adult female's body does.
Effects
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In general, androgens promote protein synthesis and growth of
those tissues with androgen receptors. Testosterone effects can
be classified as virilizing and anabolic effects, although the
distinction is somewhat artificial, as many of the effects can be
considered both. Anabolic effects include growth of muscle
mass and strength, increased bone density and strength, and
stimulation of linear growth and bone maturation. Virilizing
effects include maturation of the sex organs, particularly the
penis and the formation of the scrotum in fetuses, and after
birth (usually at puberty) a deepening of the voice, growth of
the beard and axillary hair. Many of these fall into the category
of male secondary sex characteristics.
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Testosterone effects can also be classified by the age
of usual occurrence. For postnatal effects in both
males and females, these are mostly dependent on the
levels and duration of circulating free testosterone.
Most of the prenatal androgen effects occur between
7 and 12 weeks of gestation.
Genital virilization (midline fusion, phallic urethra,
scrotal thinning and rugation, phallic enlargement)
Development of prostate and seminal vesicles
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Early infancy androgen effects are the least
understood. In the first weeks of life for male infants,
testosterone levels rise. The levels remain in a
pubertal range for a few months, but usually reach the
barely detectable levels of childhood by 4-6 months
of age. The function of this rise in humans is
unknown. It has been speculated that "brain
masculinization" is occurring since no significant
changes have been identified in other parts of the
body.
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Early postnatal effects are the first visible effects of
rising androgen levels in childhood, and occur in both
boys and girls in puberty.
Adult-type body odour
Increased oiliness of skin and hair, acne
Pubarche (appearance of pubic hair)
Axillary hair
Growth spurt, accelerated bone maturation
Fine upper lip and sideburn hair
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Advanced postnatal effects begin to occur when androgen has been higher
than normal adult female levels for months or years. In males these are
normal late pubertal effects, and only occur in women after prolonged
periods of excessive levels of free testosterone in the blood.
Phallic enlargement (including clitoromegaly)
Increased libido and erection frequency
Pubic hair extends to thighs and up toward umbilicus
Facial hair (sideburns, beard, moustache)
Chest hair, periareolar hair, perianal hair
Subcutaneous fat in face decreases
Increased muscle strength and mass
Deepening of voice
Growth of the adam's apple
Growth of spermatogenic tissue in testes, male fertility
Growth of jaw, brow, chin, nose, and remodeling of facial bone contours
Shoulders widen and rib cage expands
Completion of bone maturation and termination of growth. This occurs
indirectly via estradiol metabolites and hence more gradually in men than
women.
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Adult testosterone effects are more clearly
demonstrable in males than in females, but are
likely important to both sexes. Some of these
effects may decline as testosterone levels
decline in the later decades of adult life.
Maintenance of muscle mass and strength
Maintenance of bone density and strength
Libido and erection frequency
Mental and physical energy
Ovarian follicle
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Estrogens (mainly estradiol)
Corpus luteum
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Progesterone
Estrogens (mainly estradiol)
Placenta (when pregnant)
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Progesterone
Estrogens (mainly estriol)
Human chorionic gonadotropin (HCG)
Human placental lactogen (HPL)
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Somatostatin is secreted not only by cells of
the hypothalamus but also by delta cells of
stomach, intestine, and pancreas. It binds to
somatostatin receptors.
Somatostatin
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Somatostatin is classified as an inhibitory hormone,
whose main actions are to:
Inhibit the release of growth hormone (GH)
Inhibit the release of thyroid-stimulating hormone
(TSH)
Suppress the release of gastrointestinal hormones
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Gastrin
Cholecystokinin (CCK)
Secretin
Motilin
Vasoactive intestinal peptide (VIP)
Gastric inhibitory polypeptide (GIP)
Enteroglucagon (GIP)
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Lowers the rate of gastric emptying, and reduces
smooth muscle contractions and blood flow within
the intestine.
Suppress the release of pancreatic hormones
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Inhibit the release of insulin
Inhibit the release of glucagon
Suppress the exocrine secretory action of pancreas.
Somatostatin opposes the effects of Growth
Hormone-Releasing Hormone (GHRH)
Gonadal production of steroids. Only the ovaries have high
concentrations of the enzymes (aromatase) required to
produce the estrogens estrone and estradiol.