hormonal communication Flashcards
examples of glands in exocrine system
salivary glands (secrete saliva, containing amylase w cofactor Cl-)
liver (secretes bile, which emulsifies fats & neutralises stomach acid)
stomach (secretes gastric juice)
pancreas (secretes pancreatic juice from acinar cells)
examples of glands in endocrine system
pituitary gland (secretes ADH, which increases permeability of CD to water so increase reabsorption)
thyroid (secretes thyroxine, which regulates metabolic rate: fight/flight)
adrenal gland (secretes adrenaline and noradrenaline)
pancreas (secretes insulin and glucagon to lower or increase BGL)
ovaries (secrete oestrogen and progesterone)
testes (secrete testosterone)
what do glands do
secrete a substance
exocrine vs endocrine
exocrine: secretes substances e.g. enzymes into ducts, which open out into the body cavity
endocrine: ductless, secretes hormones directly into the blood
hormone definition
chemical messenger
produced by endocrine gland
travels in blood plasma
bind to specific target cells in organ(s)/tissue(s)
can reach whole body and effective in minute quantities
2 types of hormones
non steroid
steorid
describe properties of non-steroid hormones
water-soluble/hydrophilic/polar
do NOT enter the cell bc not lipid soluble
bind to specific, complementary receptors on cell surface membrane
examples of non steroid hormones
GLOBULAR PROTEINS eg insulin, ADH, glucagon
AMINE e.g. adrenaline, noradrenaline
properties of steroid hormones
lipid-soluble, derived form cholesterol: carried by plasma proteins
diffuse through phospholipid bilayer and bind to intracellular complementary receptors in the cytoplasm
switch on/off genes to cause response
examples of steroid hormones
testosterone, aldosterone. oestrogen, progesterone
what are non-steroid hormones known as in their mode of action
why
first messengers
they are hydrophilic so cannot pass easily through cell membrane: therefore remain outside the cell, and bind to glycoprotein receptors in the cell membrane
mode of action of non-steroid hormones
first messenger (hormone) binds to glycoprotein receptor in plasma membrane bc cannot pass through membrane as hydrophilic
cause release of another signalling molecule inside the cell (called the second messenger)
leads to a response
what is a common second messenger for non-steroid hormones
G protein
mode of action of steroid hormones
steroid hormone passes through the phospholipid bilayer bc it is lipid soluble
binds to complementary intracellular receptor in cytoplasm
forms hormone receptor complex, which acts as transcription factor
transcription factor inhibits/switches on gene
protein is produced e.g. enzyme, channel protein, hormone etc
how can one hormone have different effects on different targets
different receptor may be present
second messenger may activate different enzymes/channels
different second messengers may be activated
second messenger level may increase or decrease within the cell
location of adrenal glands
2 above kidneys
size of adrenal glands
3x5cm
5g
3 layers of adrenal cortex from outside to inside
zona glomerulosa
zona fasciculata
zone reticularis
GFR
parts of adrenal gland
adrenal cortex
adrenal medulla
type of hormone secreted by zona glomerulosa
mineral corticoids
e.g. aldosterone
aldosterone function
controls concentrations of sodium and potassium in the blood
acts on cells in the distal tubules and collecting ducts in the kidney causing increased Na+ absorption leading to increased water retention
what type of hormone does the zona fasciculata secrete
glucocorticoids
e.g. cortisol
cortisol function
helps control metabolism of carbohydrates, fats and proteins in the liver:
e.g. inhibits protein synthesis causing blood increase in amino acids
also promotes fatty acid release form adipose tissue as an energy source
released in response to stress, or low blood sugar, bc stimulates production of glucose gluconeogenesis
what type of hormone does the zona reticularis secrete
cortisol or precursor molecules of sex hormones (ANDROGENS)
e.g. oestrogen in females and testosterone in males
function of androgens
released and are converted to sex hormone which help secondary sexual characteristics develop and regulate production of gametes
what do the cells in the adrenal medulla produce
adrenaline
adrenaline structure/properties
polar molecule
derived the amino acid tyrosine
cannot pass directly across cell surface membrane so must be detected by specialised receptors in the target cell
why are the effects of adrenaline widespread
many cells and tissues have specialised adrenaline receptors
action of adrenaline on liver cells
adrenaline is hydrophilic so soluble in plasma
binds to receptor on cell surface membrane (complementary binding)
receptor changes shape, causing a G protein to be activated
G protein binds to and activates adenyl cyclase enzyme
this converts ATP into the 2nd messenger cyclic AMP
this activates other enzymes (protein kinases) which activate other enzymes (cascade effect)
this leads to a response (e.g. glycogenolysis and inhibition of glycogenesis)
why does adrenaline cause glucose to be released in a frightening situation?
muscles need glucose for respiration to release ATP to sustain muscle contraction to run away/ fight
how can the effect of adrenaline continue for hours when adrenaline only has a lifespan of 1-3 minutes in the body
adrenaline continues to be secreted form adrenal glands over a long period of time
what percentage of pancreatic tissue are the islets of langerhans
5%
parts of pancreas
islets of langerhans
pancreatic duct
acinar cells
pancreatic duct function
carries pancreatic juice to small intestine
acinar cells function
secrete pancreatic juice which drains into the duct
ducts in pancreas
intarglobular ducts feed into interlobular ducts, which feed into pancreatic duct
proportion of alpha and beta cells in islets of langerhans
more beta cells than alpha
beta cells make what
insulin, to prevent hyperglycaemia
alpha cells make what
glucagon, to prevent hypoglaecemia
how to distinguish between endocrine and exocrine tissue in pancreas
islets of langerhans (endocrine) are lightly staines, large spherical clusters which secrete and produce hormones
pancreatic acini (exocrine) are darker stained, small berry-like clusters which produce and secrete digest enzymes
name of granules in acinar cells
zymogen
2 visible features that allow you to distinguish islets of langerhans form surrounding tissue
paler than surrounding
more prominent nuclei
cells more loosely packed
bigger than surrounding acini
2 visible feature of islets of langerhans that relates to their function
contain capillaries for hormone distribution
large prominent nucleoli for secretory function
normal range for blood sugar level
4-6 mol dm-3
value of ‘too high’ blood sugar level
consistently over 7mmol dm-3
consequence of high BSL
diabetes
hyperglycaemia so glucose loss in urine so lower BP bc water lost so less blood to brain, causing a coma
value of ‘too low’ blood sugar level
consistently less than 4 mol dm-3
consequence of too low BSL
hypoglycaemia
cells run short on glucose
ketoacidosis
coma
pathway of negative feedback when BGL too high
detected by beta cells, which secrete insulin, leading to an increased uptake and respiration of glucose, increased glycogenesis, increased lipogenesis, decreased glycogenolysis and gluconeogenesis
this lowers BGL
pathway of negative feedback when BGL too low
detected by alpha cells, which secrete glucagon
increased glycogenolysis, gluconeogenesis, release of glucose and lipolysis
increased BGL
what is glycogenesis
the addition of glucose monomers to form glycogen
what is gluconeogenesis
the synthesis of glucose from non sugar precursors
what is glycogenolysis
the breakdown of glycogen into glucose
what do insulin and glucagon inhibit
the release of each other
therefore control mechanism for blood glucose levels is an example of negative feedback as BGL fluctuates around a set point
step by step insulin secretion from beta cell
cell membrane has K+ and Ca2+ ion channels, the K+ ones are normally open so K+ flow out
when BGL is too high, the glucose moves into the beta cell by FD
glucose is metabolised to produce ATP, which is used to close the K+ channels
the accumulation of K+ ions alter the potential difference across the cell membrane: the inside becomes less -ve
the change in PD opens the Ca2+ channels
Ca2+ ions caused the vesicles of insulin to fuse with the cell membrane, releasing insulin by exocytosis
how do some hormones inhibit insulin secretion
by opening K+ channels
some diabetes drugs inhibits K+ channels, so trigger insulin release
describe insulin and glucagon action
insulin binds to complementary tyrosine kinase receptor
tyrosine kinase enzyme is activated
this activates other enzymes (2nd messengers)
enzymes cause vesicles containing glut 4 transporters to move to and fuse with the membrane
glucose transporter proteins inserted into the membrane
extra glucose enters the cell by facilitated diffusion
differences between insulin and neurotransmitter secretion
cells carrying out secretion= beta cells in islets of langerhans and sensory/relay pre-synaptic neurone
stimulus= high BGL and AP transmitted along axon membrane
effect of stimulus on membrane= glucose enters cell->ATP closes K+ channels vs local current causes Na+ channels to open on synaptic knob
vesicles contain insulin vs NT
what is diabetes
common metabolic disease in humans
BGL cannot be controlled effectively
two types of diabetes proportions
10% have type 1
90% have type 2
describe type 1 diabetes
insulin dependent diabetes
begins in early life
pancreas doesn’t secrete insulin so liver cannot store excess glucose as glycogen
due to loss of B cells (caused by immune attack (autoimmune diseases)/ viral attack/ deficiency in human insulin gene)
describe type 2 diabetes
non-insulin dependent diabetes
pancreas secretes insulin but receptors on liver and muscle cells don’t respond (insulin resistance)
OR less insulin secreted due to fatty pancreas (stops B cells functioning properly)
risk factors associated with type 2 diabetes
obesity
high sugar/fat diet
genetics
lack of exercise
Asian and Afrocaribbean people have higher incidence
symptoms of diabetes
BGL remains high after high-carb meal
glucose lost in urine, so excessive urination, so dehydration, hunger and thirst
fat & proteins used as respiratory substrates, leading to ketoacidosis and low blood pH
no glycogen stores so low BGL between meals, causing hypoglycaemia bc blood sugar plummets
LT effects of diabetes
damage to blood vessels
eye and gum problems
higher risk of heart attack/ stroke. kidney failure
examples of treatment of type 1 diabetes
insulin treatments e.g. animal insulin (pig), GM bacteria
Transplants e.g. pancreas, islets of langerhans, stem-cell derived islets
advantages and disadvantages of using insulin extracted from animal pancreas e.g. pigs
A:
tried and tested method
early treatment kept people alive
D:
needs to be purified
risk of allergic reaction
high production lost
religious/ethical issues of animal products
advantages of using GM bacteria to produce human insulin
high purity
less risk of allergic reaction
lower production cost, can make large quantities to meet demand
overcomes religious/ethical issues of animal products
allows use of smart pumps/pens
pumps can be monitored by app
disadvantages of using GM bacteria to produce human insulin
people had to be persuaded to change form previous regime e.g. animal insulin
some may not understand the technology eg. injection routine (risk of hypoglycaemia if inject too much)
side effects of pumps e.g. hard lumps under skin
advantages of pancreas transplant to cure t1 diabetes
patient can now produce insulin so more physiological control of BGL
less risk of hypos and decreases longtime risk of mortality form severe hypos (hypos common if too much insulin injected)
increased QoL
80% success rate (most of the time, no need to inject)
disadvantages of pancreas transplant to cure t1 diabetes
not enough pancreases available due to donor shortage
patients require immunosuppressants for life (can lead to side effects)
use of immunosuppressant drugs leaves patients vulnerable to infections
how does transplant of islets of langerhans work
doctors use enzymes to remove islets from pancreas of organ donor
purified and counted (around 400,000 islets transplanted in each procedure)
doctors insert the cells into hepatic portal vein towards the Liver
advantages of islet transplant to treat t1 diabetes
proven curative measure
patient can now produce insulin so more physiological control of BGL
less risk of hypos and decreases longtime risk of mortality form severe hypos (hypos common if too much insulin injected)
increased QoL
slows development of diabetes complications e.g. heart diseases, kidney disease and nerve eye damage
disadvantages of islet transplant to treat t1 diabetes
limited donor supply
risk of rejection
need lifelong immunosuppressants
still classed as an experimental treatment- only performed in certain clinical trials
not all people are good candidates for transplantation. doctors must weigh up risk of taking immunosuppressants
risks to treatment e.g. bleeding and blood clots
low success rate so chance that transplanted cells may not work well/ stop working
how are iPSCs made
reprogrammed from somatic cells e.g. skin fibroblasts from diabetic patient, have similar ability to differentiate and proliferate like ESCs
ESC-derived B cells can be successfully generated by stepwise application of specific factors
how are stem cells used to treat diabetic patients?
transplant of pancreatic stem cell-derived pancreatic islet cells
immunotherapy
gene therapy
developmental biology
how are stem cells used to treat diabetic patients?: transplant of pancreatic stem cell-derived pancreatic islet cells
pluripotent stem cells could differentiate into B cells and increase the mass of the islets and increase the secretion of insulin
how are stem cells used to treat diabetic patients?: immunotherapy
pluripotent stem cells can protect B cells from autoimmune attack by inhibiting T cell proliferation and reduce the inflammatory response
how are stem cells used to treat diabetic patients?: gene therapy
opportunities to use genetic modification to provide enhanced endocrine function and survival and modulate the immune response
how are stem cells used to treat diabetic patients?: developmental biology
opportunities to study function and longevity of human islet cells with varied genotypes and develop nw drugs for treatment
advantages of using stem cells to treat t1 diabetes
no longer need to inject insulin so money saved
functioning B cells in pancreas
improved QoL
no hypoglycaemia or need for immunosuppressants
could reprogram immune system to prevent B cell damage
disadvantages of using stem cells to treat t1 diabetes
still in early stages so need more clinical trials
ethical issues with use of stem cells
risk of cancer
might still need low dose insulin
initially high cost
not suitable for all people
examples of treatment of t2 diabetes
lifestyle changes
medication
insulin therapy
treatment of t2 diabetes: lifestyle changes
losing weight
regular exercise
low sugar diet
treatment of t2 diabetes:medication
metformin acts on liver cells to decrease glucose released and increase glucose uptake
sulfonylureas stimulate pancreas ti produce more insulin
treatment of t2 diabetes: gestational diabetes
gestational diabetes affects pregnant women: high levels of glucose in blood even though normal levels of insulin produced. caused by hormones released by placenta, which prevent body using insulin effectively
TREATMENT: diet, exercise, medicines e.g. metformin, or insulin if not working
