2

020
Physi
ology of

Endocri
ne
System

M.
H De
ntal
 The Endocrine System

Types of glands in our body:

1. Exocrine gland:
 Ducts carry secretion (the secretion is not hormone) to
body surface or other organ cavity
 Extracellular effect
 Example:
o Salivary gland → saliva

o Sweat gland → sweat

o Lacrimal gland → tears

2. Endocrine gland:
 No ducts, release hormones into tissue fluid, have dense
capillary network to distribute hormones
 Extracellular effect
 Examples:
o Pituitary gland ○ Adrenal cortex
o Thyroid gland ○ Gonads testicles & ovaries
o Parathyroid gland
3. Mixed gland: pancreases

Exocrine: pancreatic duct →

Endocrine: islets of Langerhans → insulin
pancreatic juice for digestion of
and glucagon for glucose regulation
food

Note: when talking about any hormone, remember these

points:
a. Released from where (gland – cell)
b. Regulation
c. Function

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 - Metabolism: carbohydrates – lipids – protein
- Body organs
- Growth - Ions
d. Lesion
Control of hormone secretion:
1. From hypothalamus and pituitary gland
2. By feedback mechanism
How to control hormones by hypothalamus & pituitary gland
(hypothalamo-hypopheseal relationship):
1) Hypothalamus forms oxytocin & vasopressin hormones
which pass through hypothalamohypophyseal portal
tract to be stored and release in the nerve terminals
(herring bodies) of posterior pituitary gland (euro
hypophysis)
2) Hypothalamus will secrete releasing hormones which
pass through hypothalamo-hypophyseal portal
circulation to stimulate the release of trophic hormones
from anterior pituitary gland → work on target glare
examples:
Thyroid gland: thyrotropin releasing hormone →
hypothalamo-hypophyseal portal vessels → anterior
pituitary → thyroid stimulating hormone (thyrotropine) →
blood → thyroid gland → secretes T3 and T4 homrones.
When T3 and T4 increase above body needs:
- When T3, T4 ↑, they inhibit TRH & TSH "long loop
-ve feedback"
- When T5H↑, it inhibits TRH "short loop –ve
feedback"

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 - When TRH↑ it inhibits itself "ultra-short loop –ve
feedback"
 Cortex of adrenal gland: corticotropin RH → hyopthalamo-
hypophyseal portal vessels → anterior pituitary →
adrenocorticotrophic hormone → blood → adrenal cortex →
cortisol "when cortisol ↑→ -ve feedback"
 Gonads (testis in males and ovary in females) hypothalan
hypophyseal portal gate → anterior pituitary →
gonadotrophic hormones (FSH & LH) → blood → gonads
(testosterone in males – estrogen & progesterone in
females) when they increase → -ve feedback mechanism.
Non trophic hormones secreted by anterior pituitary:
Growth hormone
Growth hormone releasing hormone
Growth hormone inhibiting hormone "somatostatin"
Prolactin hormone
Prolactin releasing hormone?
Prolactin inhibiting hormone "dopamine"
Question: mention the pituitary hormones?

1) Anterior Pituitary: 2) Posterior pituitary:

 Trophic: from basophilic  Stores and releases
cells TSH, ACTH, FSH, and oxytocin vasopressin
LH (ADH)
 Non trophic: from
acidophilic cells growth
hormone & prolactin
hormone

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Oxytocin hormone:
o From para-ventricular nucleus of hypothalamus ad stored
in posterior pituitary target cell
1. Breast myoepithilial cells (contraction → milk
ejection / milk let down)
2. Uterine myometrium: causes myometrial contraction
of uterus to expel the baby n a positive feedback
mechanism:
- Stimulation of uterus by baby's head
- Hormone release from posterior pituitary
- Uterine smooth muscle contracts until baby's
birth
- Baby pushed into cervix increase hormone release
- More contraction
- When baby is born positive feedback stops
When oxytocin ↓→ no natural birth
Oxytocin increases in conditional reflex (mother thinks about
baby or hears baby cry
Prolactin hormone:
It's secreted from acidophilic cells of anterior pituitary, also
from endometriosis and placenta during pregnancy.
 Effect:
1. During pregnancy: helps to develop mammary gland
2. After pregnancy: stimulate mammary gland to produce
milk
3. Inhibits the effect of gonadotropins on ovary →
inhibits menstruation and causes infertility

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 Regulation:
o Increases by suckling (inhibits PLH → release of
prolactin)
o Increases with sleep
Prolactin secreted facilitates dopamine secretion from the
hypothalamus reducing prolactin secretion (indirect –ve
feedback)
o Increases at beginning of pregnancy and decreases at
the end of pregnancy
Antidiuretic hormone (vasopressin):
 Formed in supradoptic nucleus in the hyopothalamus, stored
and released by anterior posterior pituitary
 Target cells: kidney (distal tubules & collecting duct) →
increase water reabsorption arterioles → causes
vasoconstriction (to increase blood pressure) acts as
neurotransmitter → facilitate long-term memory
 Regulation:
Increase:
1. Increase plasma osmolarity
2. Hypouolemia (→ hypotension)
Decrease:
1. Decrease plasma osmolarity
2. Hypervolemia

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Disturbance of ADH secretion:
 Increase of ADH:
Syndrome of increase ADH (SIADH)
Due to tumour in hypothalamus
 Symptoms:
1. Increase reabsorption of water
2. Very concentrated urine
3. Edema
4. Water in toxicity (rupture of cells)
5. May lead to death
6. Decrease of ADH
7. Diabetes insipidus: inability of kidney to produce
concentrated urine it leads to:
Polyuria → dehydration (volume 4-6 L/day)
Polydipsia: increase water intake due to thirst sensation
N.B.:
The decrease of ADH may be:
Neurogenic (lesion in hypothalamus) nephrogenic (lesion
in receptors of kidney)
Remember:
1) Thyroid stimulating hormone(TSH) → from thyrotropes
- Adrenocorticotrophic hormone (ACTH) → from
corticotropes
- Growth hormone → from somatotropes
- Gonadotrophic hormones (FSH, LH) → from
gonadotropes
- Prolactin → mammotropes

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2) Long loop feedback; when target organ hormone effect
hypothalamus and pituitary (suppress trophic & releasing
hormones)
- Short loop feedback: when hormones from ant. Pituitary
effect hypothalamus
- Ultra short loop feedback: when hormones form
hypothalamus effect hypothalamus

Growth Hormone
 It's released from the acidophilic cells of anterior pituitary
gland.
 Regulation:
1. It increases in
- Hypoglycemia
- Fasting
- Exercise
- Growth hormone releasing hormone
- After meal rich n protein
- Deep sleep
- Dec. free fatty acids in blood
- Stress
2. It decreases in
- Hyperglycemia
- Aging
- Obesity
- Increased free fatty acids in blood
- Somatostatin
- Cortisol hormone

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 Function
1) On metabolism:
Carbohydrates: increase blood glucose (fasting hormone)
Lipids: lipolytic effect, increase free fatty acids formation,
by oxidation of FFAs → incr. ketone bodies formation
Protein: it is anabolic in one condition → presence of
somatomedin (from liver)
Note: in case of liver disease: growth dec. due to absence of
soamtomedin not growth hormone.
2) On growth:
Has an effect on physical growth (bone and soft tissue)
Has no effect on mental or sexual growth
Increase substance important for growth as calcium,
sodium & potassium
 Lesion:
1) Increase of growth hormone
Leads to gigantism:
o Before puberty
o Before closure of epiphysis
Leads to acromegaly:
o After puberty
o After closure of epiphysis

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 Symptoms due to GH increase:
 Increase blood glucose which causes diabetes (pituitary
diabetes
 Increase ketone bodies → ketoacidosis →coma
 Increase bone & muscle growth (length: gigantism –
thickness: acromegaly)
 Characters of gigantism:
1) Overgrowth of bone length → increase height more than
2meters
2) Overgrowth of soft tissues
3) Enlargement of internal organs
4) Diabetes mellitus
5) Hypogonadism may occur (hypersecreiton of growth
hormone may be due to tumor in pituitary gland which
may compress on other components of anterior pituitary
and dec. secretion of other hormone as ↓ gonadotropin
→ hypogonadism and delayed puberty)
6) Galactorrhea
 Characters of acromegaly:
1. Growth of bones (in width)
2. Overgrowth of soft tissues
3. Visceral enlargement
4. Ape like appearance:: (enlargement of nose, ears,
mandible and wide spaced teeth)
5. Enlargement of lips and tongue
6. Hands and feet enlargement

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 7. Peripheral nerve disorders (entrapment of nerves by
overgrowth of connective tissue and bone)
8. 25% of patients are diabetic
2) Decrease of growth hormone: causes pituitary dwarfism:
 Characters of dwarfism:
1. Height is below 120 cm
2. Symmetrical dwarfism (bone tissue and soft tissue
↓ growth)
3. Decrease in blood glucose → hypoglycemia → coma
4. Increase body weight (↓ lipolytic effect)
5. Mentally normal
6. Sexually normal

 Pituitary infertilism: due to dec. in growth hormone, FSH

and LH
Symptoms: same as pituitary dwarfism but no fertility

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 Thyroid Gland
 It consists of two lobes and isthmus between them
Each lobe consists of:
1) T hyroid follicles: follicular cells containing thyroglobulin
Inside these follicles in the thyroglobulin the thyroid hormones
are formed which are:
1. T3 tetriodotyrosin
2. T4 tetraodotyrosine
3. Reversed T3 hormone (inactive, has no function)
How are T3 $ T4 formed? In the thyroglobulin
Iodine + thyrosine → monoiodotyrosine (MIT)
2 iodine + tyrosine → dirodotyrosine (DIT)
→ MIT + DIT → T3
→ DIT + DIT → T4
After the formation of T3 and T4 → phagocytotic effect →
blood
In blood they have two forms:
1. Free: not attached to plasma protein (active form)
2. Bound: attached to plasma protein (inactive *storage+
form) so when free T3 and T4 are used the bound from
is used instead
Forms in blood: T3 = 7%" & T4 = 93%"
1. Free T3 (2%) 3. Bound T3 (98%)
2. Free T4 (0.2%) 4. Bound T4 (99.8%)

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2) Parafollicular cells: between follicular cells → secrete
calcitonin
The effects of thyroid hormones (T3 and T4)
1. On metabolism:
o Carbohydrates: increase glucose absorption in GIT,
then it decreases glucose level by glycolysis and Kreb's
cycle (for ATP production) so it has a hyperglycemic
effect at first and then hypoglycemic.
o Lipids: lipolytic effect, increase free fatty acids and
ketone bodies
o Protein: in normal level (anabolic) if increase
(catabolic)
2. On body organs:
o CNS:
 Increase maturation, brain growth , mylination of
nerves
 Increase its growth anatomically and functionally
 Increase memory and IQ *incr. maturation,
growth, function, mylenation and memory+
o Skin:
 Important for healthy skin and hair
 Normal blood supply and sweat
 Normal skin color
o CVS:
 Increase systolic blood pressure (↑ contraction
force of heart)

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  Decrease diastolic blood pressure (vasodilatation
due to ↑ metabolites)
 Increase pulse pressure
 Increase stroke volume & COP
 Increase sensitivity to catecholamine's (↑HR and
↑ contraction force)
 Cleans blood vessels from cholesterol (prevents
atherosclerosis)
o Respiratory system:
 Increase O2 utilization except in (TSALU: Testis –
spleen – adult brain, lymph nodes and uterus)
 ↑ body temp.
 ↑ mitochondria no. & function
o GIT:
 Increase motility and secretion
 Increase absorption
 Increase no. of motions
 Increase appetite and food intake
o Kidney:
 ↑ Renal flow
 ↑ Urine output
3. On growth:
o Has an effect on bone growth
o No effect on soft tissue growth
o Has an effect on mental and sexual growth

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Hyperthyroidism: (thyrotoxicosis – Grave's disease): due to
autoimmune disease → antibodies → uncontrolled stimulation
of follicular cells:
 Symptoms
1. Blood glucose suddenly → (thyroid diabetes) then
suddenly ↓ (hypoglycemia)
2. Increased appetite
3. Ketoacidosis → coma
4. Severe weight loss
5. Nervous irritation, insomnia (and tremble)
6. Exothalamus (due to formation of retro-orbital tissue),
which doesn’t disappear by treatment but needs surgery
7. Thin, vasodilated , red, hot, sweaty skin
8. Tachycardia, arrhythmia ad may cause heart failure
9. Systolic hypertension, diastolic hypotension, ↑ pulse
pressure → palpitation
10. ↑ motility of GIT →↑ no. of motions
Hyperparathyroidism: due to autoimmune disease →
antibodies → beak & attack follicular cell
1) Myxedema: (in adults)
 Symptoms:
1. Hypoglycemia
2. Always hungry (increase appetite) due to ↓ glucose
3. Gain body weight rapidly in a short time
4. Increase in cholesterol level → atherosclerosis
5. Calm cold person

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 6. Myxedema madness: lack of concentration, ↓ IQ, ↓
memory, ↓ sleep
7. Thick, cold, yellow skin with hair loss (goose skin)
8. Bradycardia, hypotension, ischemic heart
9. Constipation
2) Cretinism: (since birth)
Symptoms:
1. Asymmetric growth: ↓bone growth, normal growth
of soft tissues
2. Protruded abdomen
3. Narrow palpebral fissure
4. Pressed nose and bridge
5. Protruded tongue
6. Mentally retarded
7. Sexually retarded
Cure: Thyroid replacement therapy since birth

Parathyroid and calcitonin hormones

They are responsible for the regulation of calcium (calcium
hemostasis)
Blood calcium level is (9-11 mg/dL)
 Types of calcium in blood:
1. Free (active calcium): 50%
2. Bound (inactive calcium): 50%
- 5% in form of salt
- 45% bound to plasma protein

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 3. Main storage of free active calcium
4. Carrier of calcium
5. Prevents calcium loss in urine
 Importance of calcium:
1. 99% of calcium is found in bone and teeth
2. Important for neuromuscular transmission
3. Important for muscular contraction
4. Important for regulation of excitability (↑Ca++ →
increase rigidity of h & m gates →↓ excitability) so there
is an inverse relation bet Ca++ and excitability.
5. Important for clotting factor (no. 4)
6. Important for co-enzyme in biological activity
7. For cilia and hair cells morbility
 Regulation of calcium:
1. Parathyroid hormone (from parathyroid gland)
2. Calcitonin hormone (from extrafollicualr cells of thyroid
gland)
3. Vitamin D3: cholesterol derived steroid
 Target cells:
o Bones (reabsorption) ○ Kidney (reabsorption) ○
GIT (absorption)

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1) Effect of parathyroid hormone:
On kidney (direct and indirect)
1. Increases active form of vitamin D3 (1.25 dihydroxy
cholicalciferol)
2. Calcium is reabsorbed actively (34%) by Ca++ pump which
is activated by parathyroid hormone (from distal
convoluted tubules) (while 65% of calcium is reabsorbed
passively from proximal tubules).
3. Increase excretion of phosphate (80%↓)
(Blood calcium)  (blood phosphate) = constant –
solubility product
On bones (direct and indirect): It increases the
function of osteoclasts, osteobalasts and osteocytes
together with vitamin D3 it has two effects:
Explanation: osteoblasts and osteocytic membrane →
takes Ca++ from ECF and enter it by active uptake →
Ca++ attach to phosphate in form of hydroxy appetite
crystals → parathyroid hormones activates a pump
from the other side to take the Ca++ to blood.
Slow effect: by stimulation of osteoclasts (increase no.
& activity)
On GIT "intestine" (indirect) calcium should attach to a
protein (calbindin) → active absorption
Calbindin is formed by vitamin D3 not by parathyroid
hormone so its effect on intestine is indirect (has no
receptors in intestine)

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2) Effect of calcitonin:
 Together with vitamin D3: it's activated when Ca++ ↑
(after a meal rich in calcium) to decrease the effect of
parathyroid hormone.
 It helps in the deposition of calcium in bones (attach to
phosphate to form hydroxyl appetite crystals) so it
increases the bone strength.
 It decreases blood calcium
 The remaining calcium is excreted in urine
 Has no effect on GIT
So: Parathyroid hormone is hormone of blood calcitonin is
hormone of bones
Note: In case of old age (osteoporosis, osteomalacia) we give
them calcitonin
 Vitamin D3 injection shouldn’t be given in case of low
Ca++ (since the active hormone is parathyroid), this leads
to absorption of Ca++ from bone into blood → more bone
weakness.
 The right thing to do is: increase calcium intake (activate
calcitonin) so vitamin D3 acts to deposits Ca++ in bone →
increase bone strength.
Tetany:
 increase neuromuscular excitability due to decrease in
blood calcium level, leads to involuntary contraction of
skeletal muscles it has two types:
Manifest tetany: blood calcium below 6 gm/dL
- Generalized convulsions (in distal more than proximal)
- Laryngeal spasm (closes leading to death)

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 - Hypoparathyroidism
- Renal failure
Causes
- Alkalosis
- Decrease vitamin D3
- Cure: intravenous calcium injection very slowly
Latent tetany: blood calcium below 6 - 9 mg/dL
- Twitches from one time to other: twitches in hands
(carpal spasm): flexion in wrist, flexion in
metacarpophalengeal joint, extension in interphalnegal
joints twitches in feet (pedal spasm): arch shaped:
- Carpopedal spasm in-between attacks
- Needle sensation, tingling
 Signs:
Chovstek sign: stimulation of nerve →↑ excitability →
contraction example: tapping on angle of mandible (facial
nerve)
Erb's sign: stimulation by electrical activity.
Trousseau sign: sphygmomanometer around arm for few
minutes → spasm of muscles → carpal spasm
 Cure:
- Oral calcium
- Treatment of cause
- Vitamin D3
- If urgent I.V calcium injection

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Hyperparathyroidism (manifestation): bone, stone &
abdominal groans.
- Bones soften & deform, osteitis fibrosa cystica
- Depression of nervous system (↓ alertness, poor
memory)
- Formation of kidney stones in kidney tubules
- Cardiac arrhythmia
- Gastrointestinal disroders (peptic ulcer, nausea,
constipation)

The Adrenal Gland

There are two adrenal (suprarenal) glands one on each kidney
it consists of:
 Inner adrenal medulla (20% of the gland): Made up of
nervous tissue and acts as part of the sympathetic nervous
system. It secretes cathecholamines: epinephrine,
norephineprhin and dopamine.
 Outer adrenal cortex: (80% of the gland): consists of three
layers (zona):
- Zona glomerulosa → mineralocorticoids (aldosterone)
- Zona fasiculata → glucocorticoids (cortisol)
- Zona reticularis → sex hormones (androgen,
progesterone, estrogen)
Aldosterone: its primary target organs are distal convoluted
tubules and collecting dual of the kidney (on the Na+ - K+ pump)

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Main function: water and salt retention:
- It increases reabsorption of Na+ and Cl- (increase Na+ &
Cl- in blood)
- Increases blood volume (water increase by osmosis)
- So increases blood pressure
- Increase K+ and H+ excretion in urine (dec. K+ & H+ in
blood)
N.B.: Aldosterone also enhance sodium (Na+) absorption from
sweat, saliva, gastric juice and colon
Regulation:
It increases
- Angiotensin II "most Remember: Renin angiotensin
imp" system renin n the kidney is
- Hyponatremia sensitive to low salts and low
- Hypovolemia pressure in blood, from
- Hypotension juxtaglomerular apparatus, so it
- Hyperkalemia converts angiotensinogen in liver)
- Acidosis into angiotensin I → (in lung)
angiotensin II → gives aldosterone
It decreases:
- Arterial naturitic Remember: arterial naturitic peptide
peptide it's activated from atrium to decrease
- Hypernatremia salt and water in blood and increase
- Hypervolemia their excretion in urine → decreases
- Hypertension aldosterone secretion and decreases
- Alkalosis its effect.

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Conn's disease:
 Increase aldosterone above normal level
"hyperaldosteronism" due to tumor in zona glomerulosa
leading to:
1. Hypernatremia
2. Hypervolemia
3. Hypertension
4. Hypokameia
5. Alkalosis
Cortisol:
Effects of cortisol:
1) Metabolism:
- Carbohydrates: hyperglycemic hormone (increase
blood glucose and gluconeogenesis) one of the fasting
hormones
N.B.: fasting hormones are: growth hormone – cortisol –
glucagon
- lipids:
It has a lipolytic effect → increase ketone bodies the
lipolytidc effect is on the limbs (the excess fat is stored in
center) "so it redistributes fats"
1. Lipolytic in periphery (limbs)
2. Increase fatty acid oxidation and ketone bodies
formation
- Protein: catabolic effect except in liver (anabolic)

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2) On body organs:
CNS: Has an euphoric effect
(Has an anti-stress effect stress hormone)
It reaches its max in early morning, decreases as time
passes and reaches its minimal at night "according to
circadian rhythm"
CVS: increase blood pressure "as it increases the
sensitivity towards catecholamine's especially in blood
vessels → vasoconstriction
Lungs: bronchodilator "for treatment of bronchial
asthma"
Blood: decreases white blood cells except neutrophils
increases red blood cells and platelets
GIT: increases HCI – decreases mucosal barrier
Kidney: increases renal output so increases calcium
excretion decrease Ca++ in blood and bone
Growth decrease the effect of growth
Pharmacological effects (supraphysiological effect)
a. Bronchodilator for treatment of bronchial asthma
b. Immunosuppresor:
- Destruct lymphoid tissue and inhibits lymphocytes
- Decreases the no. of lymphocytes and antibodies
- Inhibits formation of monocytes & macrophages
- Proliferation: so it helps in decrease organ transplant
rejection and autoimmune diseases

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 Cushing syndrome: increase in cortisol hormone due to:
- Tumor in zona fasiculata
- Usage of cortisone in large doses and long time
 Symptoms:
1) Diabetes (steroid diabetes)
2) Hyperglycemia
3) Moon face and buffalo hump
4) Thin limbs and trunk obesity
5) Stretch marks are present
6) Ketoacidosis
7) Very weak bones and muscles
8) Delay of wound healing
9) Physiological problems
10) Hypertension
11) High no of RBCs (polycythemia)
12) Decreased immunity
13) Peptic ulcer
14) Gastric inflammation

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Addisonian crisis:
 The cortisol secretion doesn’t increase during stress,
trauma operations infection, saturation (↓ aldosterone,
cortisol and sex hormones).
 Symptoms:
- Hypotension: due to dec. in aldosterone and cortisol
- Hypoglycemia: due to dec. in cortisol
- Hyperkalemia
- Anemia: due to dec. in cortisol (↓ erythropoiesis)
- Vomiting and diarrhea: due to acidosis and
hyperkalemia
- Death
- Hyperpigmentation: due to increase in ACTH. The most
characteristics symptom is hypotension

Control of cortisol hormone:

- Hypothalamus: by secreting cortisol releasing hormone
(CRH) → anterior pituitary gland → secrete ACTH
Increase cortisol.

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Control of cortisol hormone:
- Hypothalamus: by secreting cortisol releasing hormone
(CRH) → anterior pituitary gland → secrete ACTH
- Negative feedback: ↑cortisol → inhibits secretion of CRH
from hypothalamus → inhibits secretion of ACTH from
anterior pituitary gland (long loop)
- Stress: increases cortisol secretion
- Circadian rhythm: the level of CRH, ACTH and cortisol in
plasma are not constant but show a diurnal fluctuation
"highest secretion in early morning, lowest in evening"

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 The Pancreas
 It’s a mixed gland: (endocrine: 1% islets of Langerhans –
exocrine: 99% pancreatic duct)
Islets of Langerhans: contain the following cells
1.  cells (5%) → glucagon
2.  cells (60%) → insulin
3.  cells (10%) → somatostatin
4. F cells (5%) → pancreatic polypeptides
Somatostatin hormone:
 It's an inhibitory hormone, secreted from hypothalamus and
 cells of pancreatic islets.
 From hypothalamus → inhibition of growth of growth
hormone
 from islets of Langerhans → inhibits insulin & glucagon
Glucagon:
 Works on liver only "hepatic effect only"
 It's an anti-insulin hormone
- On metabolism
- Carbohydrates: ↑ blood glucose by glycogenolysis from
liver
- Lipids: lipolytic effect →↑ ketone bodies (only in liver)
- Proteins: catabolic

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 Regulation:
Increase:
- ↓ blood glucose fasting hormone)
- ↑ amino acids
- Sympathetic stimulation by  receptors
- (Mild effect)
Decrease:
- Insulin
- Vagal stimulation
- Somatostatin
- Sympathetic stimulation of  receptors
- (Major effect)
Insulin hormone:
 From  cells of islets of Langerhan
 Function:
On glucose
It transport glucose from blood to the cells to:
- Store it: increase of high energy in body, it stores glucose
in the form of glycogen by glycogenesis
- Burn it: n case of low energy in body, by glycolysis
- So, it decreases blood glucose (only hypoglycemic
hormone in the body).
- It allows passage of glucose from blood by glucose
transporters as glutu which is insulin dependent in
adipose tissue & skeletal muscles

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 - The brain is insulin independent except the satiety center
note: if insulin ↓ (diabetes) no glucose enters satiety
center so the diabetic is always hungry.
On free fatty acids:
- ↑ uptake of free fatty acids and stores it in liver & adipose
tissue in the form of triglycerides. So it has a lipogenic
effect
- Note: this is why people who take insulin (not diabetics)
gain weight
Amino acids
- It allows passage of amino acids to the cells to form
protein so it has an anabolic effect, it's the most imp.
Anabolic hormone:
It forms collagen
It forms muscles
↑ growth of muscles
↑ growth of muscular organs
↑ wound healing (diabetes → delayed wound healing)
On ketone bodies:
Prevents increase of kelone bodies in blood

Note the diabetic can enter in a coma for the following

reasons
- ↑ blood glucose (hyperosmolarity – hyperglycemia)
- ↑ insulin intake (hypoglycemia)
- ↑ ketone bodies (ketoacidosis)

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Potassium:
 Prevents hyperkalemia
Hyperkalemia causes death as it arrests heart during
diastole "heart relaxes & cant contract again"
Hormones ↓ blood potassium: → insulin: → cell
→ aldosterone: → urine
 Regulation:
Increase:
- ↑ glucose (hyperglycemia)
- After food (insulin is a feasting not fasting
hormone)
- Arginine amino acid
- GIT hormones (gastrin) so insulin increases more by
glucose intake (not intravenous glucose injection),
bec. Insulin intake: 1) ↑ glucose. 2) ↑ GIT
hormones
- Glucagon
- Glucocorticoids
- Glucagon 7 cortisol inc. blood glucose during fasting
→↑ insulin
Decreases:
- Hypoglycemia
- Somatostatin
- Leptin hormone

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 Diabetes mellitus: (decrease insulin)

Insulin dependent diabetes Non-insulin independent

mellitus (type I): diabetes mellitus (type II):
- Born with weak pancreas - Insulin secretion is normal
with no sufficient insulin but receptors in the tissues
secretion (adipose tissue liver and
skeletal muscles) don’t
respond
- Treatment insulin intake - Treatment:insulin
sensitizers (oral intake)
- Occurs in extremes of age: - Happens at moderate ages:
very young – very old around 30s
- Complications are less
severe
Failure of pancreatic
pancreas change due to
since birth auto immune
disease.
Complications:
a. Diabetic coma (hyperglycemia – hypoglycemia)
b. Poly urea
c. Polyphagia: (inc. food intake due to hunger)
d. Polydipsia: (inc. water intake due to thirst)
e. Complication of other systems.

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 Nephropathy
Neuropathy: (sensory & motor)
Retinopathy: (→ unclear vision)
1. Numbness in fingers
2. Tingling in fingers
3. Decrease ability of movement
4. Gloves & stocking hypothesia.
Problems in CUS:
 causes gangrene especially in limbs
 ↑ platelets aggregation
 microvascular changes
 muscular weakness and weight loss
 delayed wound healing
Glucose homeostasis:
Normal blood glucose level is 70-110 mg%
The main organ responsible for glucose homeostasis is the
liver
Glucose is important nutrient for: brain, RBCs, retina ….

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Hormonal regulation of blood glucose level:
 Glucagon: hyperglycemic
 Catecholamines:
- Inhibits insulin & stimulates glucagons
- Stimulate glycogenolysis in muscles and liver
- Stimulatc gluconeogenesis
 Glucocorticoids:
- ↓ insulin
- ↑ glucagon's
- ↑ lipolysis (↑ glycerol for gluconeogenesis)
 Growth hormone:
- ↓ glucose uptake
- ↓ no. of glucose output
- ↑ hepatic glucose output
 Thyroid hormone:
- ↑ Glucose absorption
- ↑ Glycogenolysis
- ↑ Gluconeogenesis

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