Principles of Hormonal

Regulation
Principles of hormonal regulation
 Hormones are substances which can change
the status, function, metabolism and structure
of body organs and tissues.

 True hormones are released into blood stream

 Act only on target cells
 Active in very low doses
 May stay active for months
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 Types of hormone action
 Metabolic

 Morphogenic

 Kinetic

 Corrective
 Hormones classification
 Biochemical classification:
1. Steroids
2. Amino-acid derivatives
3. Protein-peptide compounds

 Functional classification:
1. Effectory
2. Tropic
3. Neuroregulatory (liberins & statins)
 SEQUENCE OF EVENTS INVOLVING CYCLIC
AMP AS A SECOND MESSENGER

1. The hormones combine with their receptors on the

outer surface of target cell membranes.
2. Activation of adenylate cyclase on the cytoplasmic side
of the membranes.
3. Conversion of ATP to cyclic AMP (cAMP) within the
cytoplasm.
4. cAMP activates protein kinase.
5. Protein kinase phosphorylates enzymes.
6. The activity of specific enzymes is either increased or
inhibited by phosphorylation.
7. Changes in cell metabolism, permeability or functions.
Mechanism of action of lipid solvable
hormones
Regulation of hormone secretion by the
level of effectory hormones in blood
Regulation of thyroid
hormones secretion
Regulation of sex
hormones secretion

Inhibits
sensitivity to
releasing
hormones
Thyroid gland hormones’ effects
 Increase metabolism by activating enzymes &
increasing oxygen consumption
 As the result increase heat production and
body temperature
 Morphogenic influence (especially CNS &
bone tissue)
 Activate protein synthesis by increasing
membrane permeability for amino acids
 Activate lipids breakdown
Thyroid gland hormones’ effects
 Increase glucose level in blood plasma by intensifying
glucose absorbtion in the intestines
 Activate gluconeogenesis and glucogenolysis
 Inactivate insuline by activation of liver insulinase
 Increase heart rate and cardiac output by increasing
adrenoreceptors sensitivity to adrenalin and
increasing the number of receptors
 Activate erythropoesis
Regulation of
hormone
secretion by
the regulated
parameter
 Disease States
 Both increased and decreased secretion of parathyroid hormone are
recognized as causes of serious disease in man and animals.
 Excessive secretion of parathyroid hormone is seen in two forms:
 Primary hyperparathyroidism is the result of parathyroid gland disease,
most commonly due to a parathyroid tumor (adenoma) which secretes the
hormone without proper regulation. Common manifestations of this
disorder are chronic elevations of blood calcium concentration
(hypercalcemia), kidney stones and decalcification of bone.
 Secondary hyperparathyroidism is the situation where disease outside
of the parathyroid gland leads to excessive secretion of parathyroid
hormone. A common cause of this disorder is kidney disease - if the
kidneys are unable to reabsorb calcium, blood calcium levels will fall,
stimulating continual secretion of parathyroid hormone to maintain normal
calcium levels in blood. Secondary hyperparathyroidism can also result
from inadequate nutrition - for example, diets that are deficient in calcium
or vitamin D, or which contain excessive phosphorus (e.g. all meat diets
for carnivores). A prominent effect of secondary hyperparathyroidism is
decalcification of bone, leading to pathologic fractures or "rubber bones".
 There is no doubt that chronic secretion or continuous
infusion of parathyroid hormone leads to decalcification of
bone and loss of bone mass. However, in certain
situations, treatment with parathyroid hormone can actually
stimulate an increase in bone mass and bone strength.
This seemingly paradoxical effect occurs when the
hormone is administered in pulses (e.g. by once daily
injection), and such treatment appears to be an effective
therapy for diseases such as osteoporosis.

 Inadequate production of parathyroid hormone -

hypoparathyroidism - typically results in decreased
concentrations of calcium and increased concentrations of
phosphorus in blood. Common causes of this disorder
include surgical removal of the parathyroid glands and
disease processes that lead to destruction of parathyroid
glands. The resulting hypocalcemia often leads to tetany
and convulsions, and can be acutely life-threatening.
Treatment focuses on restoring normal blood calcium
concentrations by calcium infusions, oral calcium
supplements and vitamin D therapy.
The effect of somatotropic hormone on
 protein metabolism:
1. stimulates the passing of amino acids into the cells;
2. activates the synthesis of proteins, DNA, RNA.
 carbohydrate metabolism:
1. activates the insulinase of liver;
2. inhibits the conversion of lipids to carbohydrates;
3. activates the exit of glucose from liver;
4. inhibits the entry of glucose into the cells.
 lipid metabolism:
1. stimulates lipolysis;
2. stimulates the oxidation of fatty acids.
The deficiency of somatotropic hormone in children
age causes nanism. Nanism - proportional
underdevelopment of all body.
Gigantism at
hyperproduction of STH
in children, nanism at
hypoproduction in
children
Acromegaly at hyperproduction of STH in grown-ups
 Hormones of pancreas

 Insulin. Chemical structure: protein

Effect of insulin on carbohydrate metabolism:

 increases the permeability of cell membranes of skeletal
muscles, adipose tissue and liver for glucose;
 activates the first enzyme of glycolysis - glucokinase and prevent
the inactivation of hexokinase;
 activates some enzymes of Krebs cycle (citrate synthase);
 activates the pentose phosphate cycle;
 activates glycogen synthetase;
 activates pyruvate dehydrogenase and -ketoglutarate
dehydrogenase;
 inhibits the gluconeogenesis;
 inhibits the decomposition of glycogen.
Effect of insulin on protein metabolism:
 increases the permeability of cell membranes for amino acids;
 activates synthesis of proteins and nucleic acids;
 inhibits the gluconeogenesis.
Effect of insulin on lipid metabolism:
 enhances the synthesis of lipids;
 promotes the lipid storage activating the carbohydrate
decomposition;
 inhibits the gluconeogenesis.
Effect of insulin on mineral metabolism:
 activates Na+, K+-ATP-ase (transition of K into the cells and Na
from the cells).

The deficiency of insulin causes diabetes mellitus.

Glucagon.
Chemical structure: polipeptide

Functions:
 enhances the glycogen splitting in liver;
 activates the lipolisis;
 stimulates the gluconeogenesis.
Somatostatine.
Somatostatine is produced by hypothalamus, intestine and -cells
of pancreas).
 Functions:
 inhibits the secretion of insulin and glucagon;
 inhibits secretion of somatotropic and thyrotropic hormones;
 inhibits secretion of tissue hormones of alimentary tract.
Lipocain.
Lipocain is produced in the epithelium cells of pancreatic ducts.
 Functions:
 activates the formation of phospholipids in liver and stimulates
the action of lipotropic alimentary factors;
 activates the oxidation of fatty acids in liver.
Typical findings in Cushing’s
syndrome
 Caused by prolonged decrease in plasma
corticoids
 Increased protein catabolism results in :
 Thin skin
 Poor muscle development
 Poor wound healing
 Bruisability with ecchymoses
 Thin and scraggy hair
Typical findings in Cushing’s
syndrome
 Redistribution of body fat : thin extremities, fat
collects in the abdominal wall, face, upper
back
 Purple striae (subdermal tissue rapture due to
increased subcutaneous fat depots)
 osteoporosis