Download Lect E4 - Endocrine insulin (K K DEV)

Lect E4 - Endocrine insulin
Growth, Metabolism & Calcium
Endocrine System
Summary Lect # 4
Glucose & Metabolism
1.
Growth Hormone & Somatomedins (IGF’s)
Prof Kumlesh K. Dev
Department off Physiology
h
l
2.
Thyroid hormones (T3 & T4)
3.
Oestrogens & Testosterone
4.
Mineral- (Aldosterone) & Gluco- (Cortisol) corticoids
5.
Insulin & Glucagon
6.
Calcitonin, PTH & Vit D
CRH
TRH
PRH
PIH
GnRH
dopamine
ThyrotropinReleasing
hormone
Prolactinreleasing
hormone
Prolactininhibiting
hormone
(LH releasing
hormome LHRH)
CorticotropinReleasing
hormone
GHRH
Gonadotropinreleasing
hormone
GHIH
somatostatin
Growthhormone
inhibiting
hormone
Growthhormone
releasing
hormone
ACTH
TSH
Prolactin
FSH
LH
GH
AdrenoAdrenocorticotropic
hormone
Thyroid
stimulating
hormone
(non(non-tropic)
FollicleFolliclestimulating
hormone
Luteinising
hormone
Growth
Hormone
Adrenal
cortex
Thyroid
gland
mammary
glands
cortisol
Thyroid
Hormone
(T3.T4)
breast
growth, milk
secretion
Chapter 4 Principles of Neural and Hormonal Communication
Human Physiology by Lauralee Sherwood ©2007 Brooks/Cole-Thomson Learning
many
target
organs
Ovaries
/Testes
progesterone
& estrogen
ovulation &
luteinisation
estrogen
(develop
ovarian
follicles)
testosterone
sperm
production
growth,
anabolic
actions
y
The Glands
Anabolic Steroids – Testosterone
Summary
Testosterone
• Testosterone is best known anabolic steroid
• anabolic steroids promote:
– cellll growth
h & di
division
i i
– protein synthesis
– muscle mass and strength
– appetite
– bone remodeling and growth
– production of red blood cells
• side effects of estrogen receptor activation:
– accelerated bone maturation in children
– elevated blood pressure & cholesterol levels
– mood change, acne, reduced sexual function, infertility,
testicular atrophy, baldness
1
Lect E4 - Endocrine insulin
Testosterone vs Estradiol
Feedback Loops of Estrogen/Testosterone
Testosterone
Testosterone
Testosterone ‘male’ hormone
Hypothalamus
─ fetal: for development of
reproductive organs
Gonadotroping
releasing
hormone
─ puberty: to stimulate bone growth
and secondary sexual
characteristics
GnRH
Testosterone
masculinizing hormone
Long Loop
Estradiol ‘female’ hormone
Short
Loop
─ aged: delay bone loss during
menopause
Estradiol feminizing
hormone
Gonads
Estrogen/testosterone
Growth, Metabolism & Calcium
FSH
LH
Follicle-Follicle
stimulating
hormone
Luteinising
hormone
Ovaries
/Testes
progesterone
& estrogen
ovulation &
luteinisation
estrogen
(develop
ovarian
follicles)
testosterone
sperm
production
The Glands
Summary Summary
1.
Growth Hormone & Somatomedins (IGF’s)
2.
Thyroid hormones (T3 & T4)
3.
Oestrogens & Testosterone
4.
Mineral- (Aldosterone) & Gluco- (Cortisol) corticoids
5.
Insulin & Glucagon
Calcitonin, PTH & Vit D
Ant. Pituitary
LH/FSH
─ young: stimulate growth of uterus,
sex organs, follicular growth, bone
growth
6.
GnRH
(LH releasing
hormome LHRH)
CRH
TRH
PRH
PIH
GnRH
dopamine
ThyrotropinReleasing
hormone
Prolactinreleasing
hormone
Prolactininhibiting
hormone
(LH releasing
hormome LHRH)
CorticotropinReleasing
hormone
GHRH
Gonadotropinreleasing
hormone
GHIH
somatostatin
Growthhormone
inhibiting
hormone
Growthhormone
releasing
hormone
ACTH
TSH
Prolactin
FSH
LH
GH
AdrenoAdrenocorticotropic
hormone
Thyroid
stimulating
hormone
(non(non-tropic)
FollicleFolliclestimulating
hormone
Luteinising
hormone
Growth
Hormone
Adrenal
cortex
Thyroid
gland
mammary
glands
cortisol
Thyroid
Hormone
(T3.T4)
breast
growth, milk
secretion
many
target
organs
Ovaries
/Testes
progesterone
& estrogen
ovulation &
luteinisation
estrogen
(develop
ovarian
follicles)
testosterone
sperm
production
growth,
anabolic
actions
y
2
Lect E4 - Endocrine insulin
Release of ACTH
Adrenal Gland
Adrenal Gland
Adrenal Gland
•
•
─ hypothalamus neurons in
paraventricular nucleus (PVN)
also release CRF (41 amino
acid peptide) in portal system
Adrenal cortex: outer part
CRF
•
•
•
─ CRF controls ACTH
production and release from
anterior pituitary
─ ACTH controls release of
corticosteriods from
adrenal cortex
•
•
Corticosteriods
adrenal glands embedded above each kidney in a capsule of fat
adrenals have two divisions: cortex and medulla
ACTH
Catecholamines
similar origin to gonads
make steriods hormones derived from cholesterol
Mineralocorticoids (outer, glomerulosa)
– aldosterone
Glucocorticoids (middle, fasciculata)
– cortisol (corticosterone)
Androgen sex steroids (inner, reticularis)
– DHEA (dehydroepiandrosterone)
Adrenal medulla: inner part
•
•
composed of chromaffin cells (originate from
sympathetic nervous system)
Catecholamines
– epinephrine (adrenaline)
– norepinephrine (noradrenaline)
Role of Adrenal Hormones in Metabolism
Adrenalectomy
Adrenal Gland
¾ adrenaline
¾ works in concert with sympathetic nervous system
¾ increases fat mobilisation
¾ response to stress ("fight or flight" response)
¾ cortisol released in response to ACTH
¾ stimulates hepatic gluconeogenesis
¾ inhibits tissue glucose uptake
What happens if you have no adrenal glands?
Adrenal Gland
¾ Loss of ability to respond to “stress”
¾ Loss of steroid hormones
¾ Circulatory collapse
- heart beat is less effective
- decreased peripheral resistance
- reduced cerebral blood flow
¾ Skeletal muscle fatigue
¾ Apathy
3
Lect E4 - Endocrine insulin
Mineralocorticoids – Aldosterone
Glucocorticoids – Cortisol
Adrenal Gland
Aldosterone
• is major mineralocorticoid
• Mineralocorticoids maintain body’s electrolyte
balance
Adrenal Gland
Low
Na+
and/or
high K+
• Feedback:
Angiotensin
II
– 1. low plasma Na++ or high K+
– 2. activates renin-angiotensin system
– 3. Angiotensin II increases aldosterone
release from adrenal glands
– 4. acts on distal renal tubules
• increase Na++ & water retention
• increase excretion of K+ & H+ ions
Adrenal
cortex
Aldosterone
Sex Hormones/Androgen – DHEA
Adrenal Gland
DHEA (Dehydroepiandrosterone)
• overpowered by testosterone in males
• physiologically significant in females
• supplement to gonad hormone secretion
• identical/similar to those produced by gonads
Cortisol (hydrocortisone)
• is major glucocorticoid in humans
• secretion regulated (diurnal rhythm)
– plays role in adaptation to stress
– alter glucose metabolism (inhibit glucose
uptake/use, raise blood glucose)
– alter protein & lipid metabolism (stimulates
protein breakdown, fatty acid & lipid release
in e.g.
g muscles))
– control water and electrolyte balance
– anti-inflammatory/immunosuppressive
Feedback:
• negative feedback on hypothalamus (CRH) &
anterior pituitary (ACTH)
CRH
Corticop
tropinReleasing
hormone
ACTH
Adreno-Adreno
corticotropic
hormone
Adrenal
cortex
Cortisol
Catecholamines – Nor/Adrenaline
Adrenal Gland
Epinepherine and Norepinerphrine
• Adrenal medulla is a modified part of sympathetic nervous
system
• Primary stimulus: activation of sympathetic nervous
system by stress
• Epinephrine
– Secreted into blood by exocytosis of chromaffin
g
granules
– Reinforces sympathetic system in mounting general
systemic “fight-or-flight” responses
– Maintenance of arterial blood pressure
– Increases blood glucose and blood fatty acids
4
Lect E4 - Endocrine insulin
Adrenaline and Glucocorticoids
Glucocorticoids (Cortisol) - Therapy
Adrenal Gland
Adrenal Gland
¾ Adrenal medulla – adrenaline, stored in secretory granules
¾ Adrenal cortex – cortisol, aldosterone & testosterone/oestrogens, little storage
¾ Both are important for regulation of fuel metabolism
Adrenaline
Glucocorticoids
─
─ Control of intermediate
metabolism esp gluconeogenesis
─ NOT important for rapid
mobilization of fuel
─ Important for cardiac/skeletal
muscle function
─ Anti inflammatory
─
─
─
Stimulates gluconeogenesis
and glycogenolysis
Activates hormone sensitive
lipase to promote fatty acid
release.
I
Increases
cardiac
di muscle
l
contractility
Arousal of higher centres
Glucocorticoids: hydrocortisone, prednisolone, dexamethasone, betamethasone
Replacement therapy: in adrenal failure (Addison’s disease)
A ti i fl
Anti-inflammatory/immunosuppressive
t
/i
i disorders:
di
d
reduce T cell proliferation, release of IL-2, TNF-a, IL-1
– asthma (Inhaler)
– eczema (topical cream)
– arthritis (systemic injections)
– ulcerative colitis (rectal suppositories)
– prevent graft rejection of the transplant
– cancer patients (anti-emetic; reduce oedema in brain tumours)
Benefit > Risk of glucocorticoid use
– Immune system limited (delay tissue repair, increase gastric acidity,
peptic ulcers)
– Cushinoid symptoms
– Osteoporosis (alter function of bone cells osteoblasts/osteoclasts)
– Acute adrenal insufficiency due to sudden withdrawl (patient card –
”do not stop my steroid treatment abruptly”)
Mineralocorticoids (Aldosterone) - Therapy
Addison’s disease
Adrenal Gland
Adrenal Gland
•
• fludrocortisone has g
glucocorticoid and
mineralocorticoid activity
• used in mineralocorticoid replacement
therapy (eg) in Addison’s disease.
• Kidneys
Kidneys, bladder and colon are the major
targets of mineralocorticoids
(low corticoids)
glucocorticoid (cortisol) & mineralocorticoid
(aldosterone) deficiency
Causes
• Primary Addison’s: damage of adrenal gland
(TB or autoimmunity); low cortisol and
aldosterone
•
Secondary Addison’s: low ACTH release
(when glucocorticoids are given for long periods);
low cortisol only
Symptoms
• hypoglycaemia
• decreased liver glucogen
• fatigue, anorexia, nausea, weight loss, dizziness,
hypotension, psychiatric
• death if untreated
Treatment
• Steroid replacement therapy
5
Lect E4 - Endocrine insulin
Cushing’s disease
(high glucocorticoids)
Conn’s Syndrome
(high mineralocortocoids)
Adrenal Gland
•
adrenal Hyperactivity and excess
secretion of glucocorticoids (cortisol)
Adrenal Gland
• Excessive secretion of mineralocortocoids
(aldosterone) from adrenal gland
Causes
• ACTH secreting tumor in pituitary
Causes
• primary - tumour
• secondary - excessive renin-angiotensin
action in kidney disease, cirrhosis of liver,
congestive heart failure
Symptoms
• hyperglycemia
• elevated blood pressure
• obesity (abdominal fat, thin arms & legs)
• muscle wasting, osteoporosis, cataracts
• poor wound healing
• buffalo hump, moon face, red cheeks
• psychiatric symptoms (depression,
euphoria, hallucinations)
Hyperplasia
of Adrenal Cortex
Treatment
• surgically remove adenoma, treat with
antiglucocorticoids or surgical
adrenalectomy
Symptoms
• sodium and water retention
• increase in extracellular
hypertension
fluid
Treatment
• antagonist of aldosterone
lactone)
• unilateral adrenalectomy
Hyperplastic
Normal
Stress and Depression
and
(spirono-
Cortisol Feedback
Hypothalamus-Pituitary-Adrenal (HPA) Axis
Adrenal Gland
Stress
generalised stress response
• ↑ epinephrine secretion from adrenal medulla
Higher brain centers
(chromaffin cells) for fight-or-flight response
• ↑ CRH-ACTH-cortisol
CRH ACTH cortisol (HPA axis) that mobilises
CRH
metabolic resources
• ↓ insulin & ↑ glucagon secretion to raise blood Hypothalamus Cortico-ve
tropinglucose & fatty acids
Releasing
hormone
• ↑ renin-angiotensin-aldosterone system &
from neurons
vasopressin secretion to maintain blood volume released
into blood vessels
and blood pressure
chronic stress
• causes heart disease
disease, hypertension
hypertension,
atherosclerosis, immune-suppression
• prolonged release of CRH (HPA axis
activation) causes anxiety & depression
• CRF1 receptor antagonists may treat
anxiety, depression, drug dependence
and irritable bowel syndrome
Anterior
Pituitary
ACTH
Adreno-Adreno
corticotropic
h
hormone
Adrenal Gland
Stress
Time of Day
Hypothalamus
CRH
Cortisol
CRH is released by
hypothalmic
neurosecretory cells
Long Loop
cortisol acts on CRH
neurons in
hypothalamus stops
CRH release
-ve
Ant. Pituitary
ACTH
Short Loop
Adrenal
cortex
CRH
CorticotropinReleasing
hormone
cortisol acts on
anterior pituitary
cells stops ACTH
release
CRH carried by portal
vessels into anterior
pituitary where ACTH
is released
ACTH stimulates
cortisol
ti l release
l
by
b
adrenal cortex
ACTH
Adreno-Adreno
corticotropic
hormone
Adrenal
cortex
Adrenal Cortex
cortisol
Cortisol
6
Lect E4 - Endocrine insulin
Growth, Metabolism & Calcium
Summary on Corticoids (Adrenal Cortex)
Adrenal Gland
Type
Glucocorticoids
Mineralocorticoids
N
Name
C ti l
Cortisol
Ald t
Aldosterone
Adreno-corticotropic
Hormone (ACTH)
Angiotensin II
Upstream
Hormones
Hypersecretion
Hyposecretion
Cushing’s disease
((high
g g
glucocorticoids))
Conn’s Syndrome
(high mineralocortocoids
Summary 1.
Growth Hormone & Somatomedins (IGF’s)
2.
Thyroid hormones (T3 & T4)
3.
Oestrogens & Testosterone
4.
Mineral- (Aldosterone) & Gluco- (Cortisol) corticoids
5.
Insulin & Glucagon
6.
Calcitonin, PTH & Vit D
Addison’s disease
(low corticoids)
CRH
TRH
PRH
PIH
GnRH
dopamine
ThyrotropinReleasing
hormone
Prolactinreleasing
hormone
Prolactininhibiting
hormone
(LH releasing
hormome LHRH)
CorticotropinReleasing
hormone
GHRH
GHIH
somatostatin
Growthhormone
inhibiting
hormone
Growthhormone
releasing
hormone
Gonadotropinreleasing
hormone
ACTH
TSH
Prolactin
FSH
LH
GH
AdrenoAdrenocorticotropic
hormone
Thyroid
stimulating
hormone
(non(non-tropic)
FollicleFolliclestimulating
hormone
Luteinising
hormone
Growth
Hormone
Adrenal
cortex
Thyroid
gland
mammary
glands
cortisol
Thyroid
Hormone
(T3.T4)
breast
growth, milk
secretion
many
target
organs
Ovaries
/Testes
progesterone
& estrogen
ovulation &
luteinisation
estrogen
(develop
ovarian
follicles)
testosterone
sperm
production
growth,
anabolic
actions
y
The Glands
Metabolism
Summary
Body Fuel ─
energy requirements vary during
sleep, exercise, illness, starvation
─
energy expenditure
dit
and
d ffuell supply
l
regulated by endocrine system
─
protein, carbohydrate, and fat in
diet are broken down into
intermediates that are convertible
─
used for two purposes
Carbohydrate
Protein
Fat
Glucose
Amino Acids
Fatty Acids
Pyruvate
Oxaloacetate
AcCoA
─ 1. energy production
─ 2. tissue growth & repair
─
Krebs cycle
i.e. hormones control normal fuel
supply, growth and development
ATP
7
Lect E4 - Endocrine insulin
Hungry vs. Fed
Starvation
Body Fuel protein
glycogen
Hungry State
Muscle
glucose
(in)
glycogen
amino acids
(out)
glycerophosphate
ketoacids
triglyceride
(in)
amino acids
(in)
glucose
(in)
fatty acid
glycerophosphate
triglycerides
(in)
pyruvate
(in)
starvation reduces energy
expenditure/metabolic rate
glucose
─
circulating glucose,
glucose fatty acid
and triglycerides in body provide
energy for ~ 1-2 hrs
C l ifi value
Calorific
l
off substrates
b t t
are:
• Glucose
17.6 kJ/g
• Amino acids
18.0 kJ/g
• Fatty acids
39.0 kJ/g
─
glycogen store in liver and
muscle provide 800 kcal (~8 hrs
fuel)
pyruvate (out)
glucose
(out)
fatty acid
─
glycogen
protein
glucose
(in)
Liver
Factors affecting stores
─ growth
─ feeding - need energy for
absorption, digestion
─ between meals,
meals overnight
─ starvation, long term (weeks) or
short term (days)
─ disease, trauma, infection,
surgery
─ pregnancy
Fed State
amino acids
(in)
Adipose
─ fed state: store amino acids,
glucose and triglycerides
─ hungry
h
state:
t t mobilise
bili stored
t d
reserves
Body Fuel Adult body uses following per day:
• Glucose
250g
• Amino acids
150g
• Fatty acids
100g
glycerol
glycogen
amino acids
(in)
fatty acids
(in)
ketoacids
ketones
(out)
triglycerides
fatty acids
(out)
glycerol
─
─
during
g fasting
g triglycerides
gy
metabolised; fat stores hold
100,000 kcal (30 days)
when fat stores exhausted,
protein breakdown provides
10,000 kcal; muscle wasting
Feeding
Total = 11MJ/day
Starvation in 70kg adult
¾ 35kg muscle (7 kg protein)
¾ 20% body fat (14 kg)
¾ 400 g glycogen
¾ Resting Metabolic Rate 10MJ/d
How long before death?
¾
Protein
= 126MJ
¾
Fat
= 546MJ
¾
CHO
= 7.2MJ
¾
Total
= 679 MJ = 68d
Note: not all protein, fat can be used
(cell memb)
Exercise
Body Fuel Body Fuel ─ feeding increases fat,
g
amino acids & glucose
in blood
─ increases sympathetic stimulation
─ increases
i
glucagon
l
─ decreases insulin
─ release insulin &
decrease glucagon
─ increases adrenaline
─ increases glucose and fuel output
─ if meal is mostly protein
then glucagon also
i
increases
─ takes several hours for
hormonal response to
subside
─ suppressed
pp
storage
g
─ increases glucose uptake into muscle
Well
fed
2 wks
starved
6μU/ml
¾
INSULIN
40μU/ml
¾
GLUCAGON
80 pg/ml
120 pg/ml
¾
GLUCOSE
6 mM
3.6 mM
8
Lect E4 - Endocrine insulin
Hormones Regulating Metabolism
Islets of Langerhans
Body Fuel ─ Anterior Pituitary gland
─ Growth hormone, ACTH, TSH
─ Liver
Insulin/Glucagon ─
pancreas exocrine and endocrine cells
─
exocrine cells secrete proteases into small
intestine
─
Endocrine Islet of Langerhans
─ comprise 1 % of pancreas
─ rich blood supply for hormone drainage
─ clusters composed ~3000 endocrine
secretory cells
─ surrounded
d db
by capsule
l
─ scattered throughout pancreas
─
pancreas removal causes symptoms of
diabetes
─ ↑ [glucose]plasma 20-30mM
─ Somatomedins (IGF’s)
─ Thyroid gland (T3 T4 )
─ Thyroxine
─ Gonads
─ Sex steroids
─ Adrenal cortex
─ Glucocorticoids (cortisol)
─ Adrenal medulla
─ adrenaline (noradrenaline)
─ Pancreatic (Islets of Langerhans)
─ Insulin & glucagon
Islets of Langerhans – Cell & Hormones
Islets of Langerhans – Cell & Hormones
Insulin/Glucagon ─ islets of Langerhans have 3 secretory
cells producing peptide hormones
Insulin/Glucagon Cell Type
Hormone
Role
beta β cells
insulin
promotes glucose uptake
decrease glucose in blood
(see next slide)
─ α cells - glucagon - opposite
effect to insulin
alpha α cells
glucagon
─ δ cells – somatostatin potentiates
t ti t glycogen
l
breakdown
b kd
activity of glucagon
opposite effect to insulin
promotes blood glucose levels
(see next slide)
delta δ cells
somatostatin
potentiates glycogen breakdown
activity of glucagon
(see growth hormone inhibitory hormone)
─ β cells - insulin - promotes
glucose uptake
─ insulin stored in & secreted from
cytoplasmic granules
VERY VERY IMPORTANT
VERY VERY IMPORTANT
9
Lect E4 - Endocrine insulin
Effects of Insulin & Glucagon
Pro-Insulin & Insulin
Insulin/Glucagon Insulin
¾
¾
¾
¾
¾
Insulin/Glucagon Glucagon
fed state: anabolic hormone
¾ glucose to glycogen
¾ fatty acids to triglycerides
¾ amino acid to protein
↑ enzymes in liver & muscle to
convert glucose to glycogen
↑ uptake of glucose from blood into
muscle and fat
↑ incorporation of amino acids into
protein in muscle
↓ lipolysis & promotes lipogenesis in
adipose tissue
glycogenolysis/lytic
gluconeogenesis
lipolysis
lipogenesis
¾
¾
¾
¾
¾
¾
¾
¾
¾
¾
hungry state: catabolic hormone
¾ glycogen to glucose
¾ triglycerides to fatty acids
↑ hepatic glycogen breakdown
↓ hepatic glycogen synthesis
↑ hepatic glucose synthesis
↓ amino acid uptake in muscle
↑ amino acid uptake by liver
↑ liver deaminates amino acids,
converting
ti to
t glucose
l
↑ glucose levels & insulin secretion
↑ adrenaline release
↑ lipolysis in liver & adipose tissue
– glycogen breakdown
– glucose synthesis
– lipid/fat breakdown
– lipid/fat synthesis
Factors regulating insulin release
¾ insulin synthesised as prohormone which is cleaved
to mature peptide in secretory granules
¾ insulin and glucagon have short half life so need
sustained release to maintain serum concentration
¾ insulin
glucagon
t1/2 = 30 minutes
t1/2 = 10 minutes
Glucose Transporter
Insulin/Glucagon Promoting secretion
¾
¾
¾
¾
↑ glucose
↑ parasymp’ activity
↑ amino acids (arginine)
↑ glucagon
Inhibiting secretion
¾
¾
¾
¾
↓ glucose
↑ sympathetic activity
↑ somatostatin release
↑ cortisol
Insulin/Glucagon ─ insulin causes glucose
transporters to be inserted
in plasma membrane
─ this increases glucose
uptake by muscle and
adipose tissue
─ reduces blood glucose
levels
10
Lect E4 - Endocrine insulin
Diabetes Mellitus
Effects of severe diabetes
Insulin/Glucagon Type II Diabetes
¾ symptoms develop rapidly
symptoms develop slowly
¾ childhood onset
adulthood onset
¾ affects 10-20% diabetics
affects 80-90% diabetics
¾ loss of β cell function
insulin insensitivity
¾ insulin secretion none/low
insulin secretion normal or high
¾ insulin injections for treatment
diet/exercise and oral drugs
1. excessive eating
¾ cells starved of carbohydrate
¾ hypothalamic center leads to excessive eating
2. dehydration and thirst
¾ low glucose uptake, blood glucose rises
¾ exceeds renal filtration capacity
¾ glucose appears in urine, increases urinary vol
¾ dehydration and thirst
Glucose Tolerance
Test
Blood Sugar mg/dl
Type I Diabetes
Insulin/Glucagon 300
Diabetes
200
3. coma
¾ cells unable to use glucose increases
100
¾ lipolysis to generate fatty acids
¾ fatty acids metabolism → acetyl CoA → ketoacids
¾ ketoacids lower blood pH
¾ hyperventilation to maintain blood pH
¾ decreased brain O2 and coma
Normal
1
2
Hours
3
4. brain cells are glucose obligate cells
¾ low glucose, brain stops working
¾ coma and respiratory paralysis
Growth, Metabolism & Calcium
Insulin & Glucagon Feedback loops
Summary Insulin/Glucagon 1.
Growth Hormone & Somatomedins (IGF’s)
2.
Thyroid hormones (T3 & T4)
3.
Oestrogens & Testosterone
4.
Mineral- (Aldosterone) & Gluco- (Cortisol) corticoids
5.
Insulin & Glucagon
6.
Calcitonin, PTH & Vit D
CRH
TRH
PRH
PIH
GnRH
dopamine
ThyrotropinReleasing
hormone
Prolactinreleasing
hormone
Prolactininhibiting
hormone
(LH releasing
hormome LHRH)
CorticotropinReleasing
hormone
GHRH
Gonadotropinreleasing
hormone
GHIH
somatostatin
Growthhormone
inhibiting
hormone
Growthhormone
releasing
hormone
ACTH
TSH
Prolactin
FSH
LH
GH
AdrenoAdrenocorticotropic
hormone
Thyroid
stimulating
hormone
(non(non-tropic)
FollicleFolliclestimulating
hormone
Luteinising
hormone
Growth
Hormone
Adrenal
cortex
Thyroid
gland
mammary
glands
cortisol
Thyroid
Hormone
(T3.T4)
breast
growth, milk
secretion
many
target
organs
Ovaries
/Testes
progesterone
& estrogen
ovulation &
luteinisation
estrogen
(develop
ovarian
follicles)
testosterone
sperm
production
growth,
anabolic
actions
y
11