3.6.4 Homeostasis

homeostasis

the maintenance of constant internal environment in the body

importance of maintaining stable core temperature

maintains stable rate of enzyme-controlled reactions by maintaining optimum temperature (37C)

-if temp is too low = enzyme + substrate have insufficient kinetic energy so fewer collisions so fewer E-S complexes

-if temp is too high = enzymes denature so slow rate

thermoregulation

-change in temperature is detected by thermoreceptors in skin and by hypothalamus

-hypothalamus coordinates response to change by sending nerve impulses to effectors

thermoregulation -if body temp INCREASES

-blood vessels in skin dilate allowing more heat to be radiated = vasodilation

-sweat is released from glands so will evaporate and cool the skin due to high latent heat of vaporisation of water 

-so body temp decreases to normal

thermoregulation -if body temp DECREASES

-blood vessels in skin constrict reducing heat loss = vasoconstriction

-sweat glands stop releasing sweat + skeletal muscles contract and shiver, generating heat by respiration

-so body temp increases to normal

endotherm vs ectotherm animals

-endotherm = ‘warm blooded’, high metabolism = more respiration, maintain same body temp

-ectotherm = ‘cold blooded’, low metabolism = less respiration, equilibrates/adapts to temp of surroundings

negative feedback

-effectors maintain a constant level

-fluctuates around constant

e.g. thermoregulation

positive feedback

-effectors further increase level away from constant/normal

-stimulate more impulses to be sent to carry out

e.g. pregnancy contractions

importance of glucose regulation

-maintains constant blood water potential = prevents osmosis lysis of cells

-maintains constant concentration of respiratory substrate = glucose is a vital substrate for brain cells, maintains constant level of activity

pancreas

-glucagon = secreted by alpha cells, found in islets of Langerhans, increases blood glucose conc

-insulin = secreted by beta cells, found in islets of Langerhans, decreases blood glucose conc

key processes in liver

-glycogenesis = formation of glycogen from glucose, stimulated by insulin, decreases blood glucose

-glycogenolysis = breakdown of glycogen into glucose, stimulated by glucagon + adrenaline, increases blood glucose

-gluconeogenesis = synthesis of new glucose from amino acids + fats, stimulated by glucagon, increases blood glucose

when blood glucose conc INCREASES -hyperglycaemia 

-hypothalamus + islets of Langerhans in pancreas detects

-beta cells release insulin in blood

-insulin bind to specific receptors on target cells which trigger insertion of GLUT4 transport proteins, making membrane more permeable to glucose

-more glucose moves in and insulin activates enzymes to stimulate glycogenesis in the liver

-insulin increases rate of glucose used by body cells in respiration

-blood glucose level declines

when blood glucose conc DECREASES -hypoglycaemia

-hypothalamus + islets of Langerhans in pancreas detects

-alpha cells release glucagon in blood

-glucagon binds to specific receptors on target cells and activates enzymes to stimulate gluconeogenesis

-glucagon also activates enzymes to stimulate glycogenolysis by the liver

-blood glucose level rises

adrenaline

-released by adrenal glands during stress or excitement

-increases blood glucose conc + uses second messenger model = binding of hormone to receptors which activate an enzyme on inside to then produce chemical

process of adrenaline

1) first messenger - adrenaline binds to specific receptors on target cells which activate protein inside cell which then activates enzyme adenylate cyclase

2) second messenger - enzyme converts ATP into cyclic AMP (cAMP)

3) cAMP activates enzyme protein kinase which intiates enzyme cascade

4) eventually activates enzymes for glycogenolysis + inhibits enzymes involved in glycogen synthesis

5) so glucose is released into liver

type 1 diabetes

-autoimmune response where the body’s immune system attacks + destroys the beta cells in islets of Langerhans

-none or very little insulin produced

-usually develops quickly in childhood or adolescence

-control = insulin injections, controlled diet

type 2 diabetes

-target cell receptors become less responsive to insulin produced by pancreas or pancreas produces insufficient insulin

-can be normal insulin production but is ineffective

-usually develops slowly in older adults

-control = lifestyle changes