5.1.4 Hormonal Communication
Endocrine communication
secretion of hormones into blood from endocrine glands; consists of group of cells that manufacture hormones and release them; ductless glands
transport by blood in capillaries
detection by target cells or tissues; hormone binds to receptors on target cells or tissues which initiates changes in the cell
Adrenal glands
Pancreas
Regulating blood glucose concentration
Diabetes mellitus
Type 1
treatment: insulin injections, insulin pump therapy (needle that is permanently injected in skin pumps insulin constantly), islet cell transplantation (beta cells are transplanted from a dead person), pancreas transplant
Type 2
causes: obesity, low fitness levels, no exercise, genetic, diet high in sugar, family history
treatment: change in lifestyle; lose weight, exercise, monitor diet; if severe then insulin injections
potential treatments
sources of insulin: E. coli bacteria is genetically modified to produce human insulin
stem cells: grow new beta cells in islets of Langerhans in pancreas
Sammer Sheikh
Endocrine system: a communication system using hormones as its signalling molecules
target cells: for non-steroid hormones; cells that possess a specific receptor on their plasma membrane; shape of receptor is complementary to shape of hormone molecule; many similar cells form a target tissue
Hormones
molecules (proteins or steroids) that are released by endocrine glands directly into the blood; act as messengers by carrying a signal from the gland to a specific target organ or tissue
protein and peptide hormones, derivative of amino acids e.g. adrenaline, insulin, glucagon; insoluble in phospholipid bilayer so need to bind to plasma membrane and release a second messenger inside the cell
steroid hormones e.g. oestrogen, testosterone; pass through membrane and enter cell and nucleus; direct effect on DNA
Messengers
First messengers: non-steroid hormones; bind to plasma membrane and do not enter cell; release secondary messenger
Second messengers: steroid hormones; stimulates change in activity of cell
G-protein
is activated when first messenger binds to receptor
activates effector molecule e.g. an enzyme (e.g. adenyl cyclase) that converts an inactive molecule (e.g. ATP) into a secondary messenger (e.g. cAMP) which may effect another protein directly or initiate cascade of enzyme reactions
insulin:
hormone released from beta cells in the pancreas that decrease blood glucose concentrations
more transporter proteins specific to glucose are places into cell surface membranes; vesicles containing these fuse with membrane
more glucose enters cell
glycogenesis: glucose is converted to glycogen for storage
more glucose converted to fats
more glucose used in respiration
If blood glucose too high:
insulin is released by beta cells in islets of Langerhans in pancreas
increased uptake of glucose through specific transport proteins reduces blood glucose concentration
insulin binds to receptor on cells (muscle and liver) and activated enzyme tyrosine kinase
tyrosine kinase causes phosphorylation of inactive enzymes in cell; cascade of enzyme controlled reactions in cells
glucagon
hormone released from alpha cells in the pancreas that increase blood glucose concentration
glycogenolysis: glycogen is converted to glucose by phosphorylase A (enzyme activated in cascade)
more fatty acids used in respiration
gluconeogenesis: amino acids and fats are converted to additional glucose
If blood glucose too low:
glucagon is released by alpha cells in islets of Langerhans in pancreas
glucagon binds to receptor on hepatocytes (in liver) and stimulated a G protein inside membrane
G protein activated adenyl cyclase; converts ATP to cAMP; cascade of enzyme controlled reactions in cells
increase blood glucose concentration
inhibit glucagon
inhibit insulin
a condition in which blood glucose concentration cannot be controlled effectively; cannot produce sufficient insulin so causes hyperglycemia after eating and hypoglycemia after fasting
causes: autoimmune response attacks and destroys beta cells, in childhood, viral attack,
can synthesise sufficient insulin
can produce insulin but not enough, cells lose receptors on surface of liver and muscle cells with age; blood glucose is almost always high
exact copy of human insulin; faster acting and more effective
less chance of developing tolerance
less chance of autoimmune rejection
lower risk of infection
cheaper to manufacture than to extract it from animal
less moral dilemmas
Advantages:
adrenal cortex
use cholesterol to produce hormones; steroid based so are able to dissolve directly into plasma membrane
steroid hormone passes through plasma membrane of target cell and binds to receptor in cytoplasm; receptor-steroid complex enters nucleus and binds to another specific receptor on chromosomal material; stimulates production of mRNA
zona glomerulosa: release glucocorticoids: control metabolism of carbs, fats and proteins in the liver e.g. cortisol released in response to stress or low blood sugar; stimulates production of glucose from steroid compounds (glycogen, fats, proteins) in the liver
zona fasciculata: secrete mineralocorticoids: control Na⁺ and K⁺ concentration in blood; maintain blood pressure e.g. aldosterone acts on cells of distal tubules and collecting ducts to decrease absorption of K⁺ ions and increase absorption of Na⁺ to increase water retention and blood pressure
zona reticularis: if correct enzymes not present for release of cortisol then precursor androgens are released into blood; converted to sex hormones in ovaries or testes; help development of secondary sexual characteristics and regulate production of gametes
adrenal medulla
adrenaline: "fight or flight"; protein hormone so cannot pass through plasma membrane; increase heart rate and stroke volume, dilate pupils, vasoconstriction to raise blood pressure; increase mental awareness; glycogenolysis
noradrenaline: similar to adrenaline, but mostly a neurotransmitter as it is released mostly in brain; increase heart rate etc
structure:
endocrine function: hormones released directly into blood to control blood glucose concentration
exocrine function: pancreatic juice is released into a duct, into the duodenum of small intestine
beta cells: found in islets of Langerhans; secrete insulin
alpha cells: found in islets of Langerhans; secrete glucagon
exocrine cells are in small groups surrounding tubules called an acinus; cells of acini secrete enzymes into tubule in centre; tubules join up to form duct
pancreatic juice contains digestive enzymes (amylase, lipase and protease) and sodium hydrogencarbonate to make it alkaline
Insulin secretion
1) K⁺ channels of beta cells are usually open so K⁺ ions flow out and make water potential of cell more negative; Ca²⁺ channels are usually closed so Ca²⁺ ions cannot enter
2) glucose moves into the cell if blood glucose concentration is too high
3) glucose is converted to produce ATP by enzyme glucokinase
4) extra ATP causes K⁺ channel to close
5) K⁺ cannot flow out so water potential of cell becomes less negative
6) Ca²⁺ ion channels opens so Ca²⁺ ions diffuse into the cell
7) Vesicles containing insulin fuse with cell surface membrane so insulin is released by exocytosis