[3.6] Organisms Respond to Changes in their Internal & External Environments

Question 1

What is a stimulus?

Answer 1

A change in an organism’s internal or external environment.

Question 2

Why is it important that organisms can respond to stimuli?

Answer 2

Organisms increase their chance of survival by responding to stimuli.

Question 3

What is a tropism?

Answer 3

• Growth of a plant in response to a directional stimulus.
• Positive tropism = towards a stimulus; negative tropism = away from stimulus.

Question 4

Summarise the role of growth factors in flowering plants.

Answer 4

• Specific growth factors (hormone-like growth substances) e.g. Auxins (such as IAA) move (via phloem or diffusion) from growing regions e.g. shoot / root tips where they’re produced.
• To other tissues where they regulate growth in response to directional stimuli (tropisms).

Question 5

Describe how indoleacetic acid (IAA) affects cells in roots and shoots.

Answer 5

• In **shoots*, high concentrations of IAA stimulates cell elongation.
• In roots, high concentrtions of IAA inhbitis cell elongation.

Question 6

Explain gravitropism in flowering plants.

Answer 6

1. Cells in tip of shoot / root produce IAA.
2. IAA diffuses down shoot / root (evenly initally).
3. IAA moves to lower side of shoot / root (so concentration increases).
4. In **shoots* this stimulates cell elongation whereas in roots this inhbits cell elongation.
5. So shoots bend away from gravity wheras roots bend towards gravity.

Question 7

Explain phototropism in flowering plants.

Answer 7

1. Cells in tip of shoot / root produce IAA.
2. IAA diffuses down shoot / root (evenly initally).
3. IAA moves to shaded side of shoot / root (so concentration increases).
4. In shoots this stimulates cell elongation whereas in roots this inhibits cell elongation.
5. So shoots bend towards light whereas roots bend away from light.

Question 8

Describe the simple responses that can maintain a mobile organism in a favourable environment.

Answer 8

1. Taxes (tactic responses).
   
   • Directional response.
   • Movement towards or away from a directional stimulus.
2. Kinesis (kinetic responses).
   
   • Non-directional response.
   • Speed of movement or rate of direction change changes in response to a non-directional stimulus.
   • Dependning on intensity of stimulus.

Question 9

Explain the protective effect of a simple (e.g. 3 neurone) reflex.

Answer 9

• Rapid as only 3 neurones and few synapses (synaptic transmission is slow).
• Autonomic (doesn’t involve conscipus regions of brain) so doesn’t have to be learnt.
• Protects from harmful stimuli e.g. escape predators / prevents damage to body tissues.

Question 10

Describe the basic structure of a Pacinian Corpuscle

Answer 10

Question 11

Describe how a generator potential is established in a Pacinian corpuscle.

Answer 11

1. Mechanical stimulus e.g. pressure deforms lamellae and stretch-mediated sodium ion (Na⁺) channels.
2. So Na⁺ channels in membrane open and Na⁺ diffuse into sensory neurone.
   
   • Greater pressure causes more Na⁺ channels to open and more Na⁺ to enter.
3. This causes depolarisation, leading to a generator potential.
   
   • If a generator potential reaches threshold, it triggers an action potential.

Question 12

Explain what the Pacinian corpuscle illustrates.

Answer 12

• Receptors respond only to specific stimuli.
  
  • Pacinian corpuscle only responds to mechanical pressure.
• Stimulation of a receptor leads to the establishment of a generator potential.
  
  • When threshold is reached, action potential sent (all-or-nothing principle).

Question 13

Explain the difference in sensitivity to light for rods & cones in the retina.

Answer 13

Rods are more sensitive to light

• Several rods connected to a single neurone.
• Spatial summation to reach / overcome threshold (as enough neurotransmitter released) too generate an action potential.

Cones are less sensitive to light

• Each cone connected to a single neurone.
• No spatial summation.

Question 14

Explain the difference in visual acuity for rods & cones in the retina.

Answer 14

Rods give lower visual activity

• Several rods connected to a single neurone.
• So several rods send a single set of impulses to brain (so can’t distinguish between separate sources of light).

Cones give higher visual acuity

• Each cone connected to a single neurone.
• Cones send separate (sets of) impulses to brain (so can’t distinguish distinguish between 2 separate sources of light)

Question 15

Explain the differences in sensitivity to colour for rods & cones in the retina.

Answer 15

Rods allow monochromatic vision

• 1 type of rod / 1 pigment.

Cones allow colour vision

• 3 types of cones - red-, green- and blue-sensitive.
• With different optical pigments -> absorb different wavelengths.
• Stimulating different combinations of cones gives range of colour perception.

Question 16

The cardiac muscle is myogenic. What does this mean?

Answer 16

• It can contract and relax without receiving electrical impulses from nerves.

Question 17

Label the sinoatrial node (SAN), atrioventricular node (AVN), Bundle of His and Purkyne tissue on a diagram of the heart.

Answer 17

Question 18

Describe the myogenic stimulation of the heart and transmission of a subsequent wave of electrical activity.

Answer 18

1. Sinoatrial node (SAN) acts as pacemaker -> releases regular waves of electrical activity across atria.
   • Causing atria to contract simultaneously.
2. Non-conducting tissue between atria / ventricles prevents impulses passing directly to ventricles.
   • Preventing immediate contraction of ventricles.
3. Waves of electrical activity reach atrioventricular node (AVN) which delays impulse.
   • Allowing atria to fully contract and empty before ventricles contract.
4. AVN sends wave of electrical activity down bundle of His, conducting wave between ventricles to apex where it branches into Purkyne tissue.
   • Causing ventricles to contract simultaneously from the base up.

Question 19

Where are chemoreceptors and pressure receptors located?

Answer 19

• Chemoreceptors and pressure receptors are located in the atria and carotid arteries.

Question 20

Describe the role of chemoreceptors, pressure receptors, the autonomic nervous system and effectors in controlling heart rate when a fall in blood pressure OR rise in blood CO2 conc. / fall in blood pH is detected.

Answer 20

1. Baroreceptors detect fall on blood pressure and / or chemoreceptors detect blood rise in blood CO2 conc. or fall in blood pH.
2. Send impulses to medulla / cardiac control centre.
3. Which send more frequent impulses to SAN along sympathetic neurones.
4. So more frequent impulses sent from SAN and to / from AVN.
5. So cardiac muscle contracts more frequently.
6. So heart rate increases.

Question 21

Describe the role of chemoreceptors, pressure receptors, the autonomic nervous system and effectors in controlling heart rate when a raise in blood pressure OR fall in blood CO2 conc. / rise in blood pH.

Answer 21

1. Baroreceptors detect rise on blood pressure and / or chemoreceptors detect blood fall in blood CO2 conc. or rise in blood pH.
2. Send impulses to medulla / cardiac control centre.
3. Which send more frequent impulses to SAN along parasympathetic neurones.
4. So less frequent impulses sent from SAN and to / from AVN.
5. So cardiac muscle contracts less frequently.
6. So heart rate decreases.

Question 22

Describe the structure of a myelinated motor neurone.

Answer 22

Question 23

Describe resting potential.

Answer 23

• Inside of axon has a negative charge relative to outside (-70mV).
  
  • i.e. more positive ions outside compared to inside.

Question 24

Explain how a resting potential is established across the axon membrane in a neurone.

Answer 24

• Na⁺/K⁺ pump actively transports:
  
  • 3 Na⁺ out of axon AND 2 K⁺ into axon.
• Creating an electrochemical gradient:
  
  • Higher K⁺ concentration inside AND higher Na⁺ concentration outside.
• Differential membrane permeability:
  
  • More permeable to K⁺ -> move out by facilitated diffusion.
  • Less permeable to Na⁺ (closed channels).

Question 25

Explain how changes in membrane permeability lead to deplorisaiton and the generation of an action potential.

Answer 25

1. Stimulus.
   
   • Na⁺ channels open; membrane permeability to Na⁺ increases.
   • Na⁺ diffusion into axon down electrochemical gradient (causing depolarisation).
2. Depolarisation.
   
   • If threshold potential is reached, an action potential is generated.
   • As more voltage-gated Na⁺ channels open (positive feedback effect).
   • So more Na⁺ diffuse in rapidly.
3. Repolarisation.
   
   • Voltage-gated Na⁺ channels close.
   • Voltage-gated K⁺ channels open; K⁺ diffuse out of axon.
4. Hyperpolorisation.
   
   • K⁺ channels slow to close so there’s a slight overshoot = too many K⁺ diffuse out.
5. Resting potential.
   
   • Restored by Na⁺/K⁺ pump.

Question 26

Draw and label a graph showing an action potential.

Answer 26

Question 27

Describe the all-or-nothing principle.

Answer 27

• For an action potential to be produced, depolarisation must exceed threshold potential.
• Action potentials produced are always same magnitude / size / peak at same potential.
  
  • Bigger stimuli instead increase frequency of action potentials.

Question 28

Describe the nature of the refractory period.

Answer 28

• Time taken to restore axon to resting potential when no further action potential can be generated.
• As Na⁺ channels are closed / inactive / will not open.

Question 29

Explain the importance of the refractory period.

Answer 29

• Ensures discrete impulse are produced (action potentials don’t overlap).
• Limits frequency of impulse transmission at a certain intensity (prevents over reaction to stimulus).
  
  • Higher intensity stimulus causes higher frequency of action potentials.
  • But only up to certain intensity.
• Also ensures action potentials travel in one direction - can’t be propagated in a refractory region.

Question 30

Explain how the passage of an action potential along non-myelinated and myelinated axons result in nerve impulses.

Answer 30

NON-MYELINATED AXON

• Action potential passes as a wave of depolarisation.
• Influx of Na⁺ in one region in increases permeability of adjoining region to Na⁺ by causing voltage-gated Na⁺ channels to open so adjoining region depolarises.

MYELINATED AXON

• Myelination provides electrical insulation.
• Depolarisation of axon at nodes of Ranvier only resulting in saltatory conduction (local currents circuits).
• So there is no need for depolarisation along whole length of axon.

Question 31

Suggest how damage to the myelin sheath can lead to slow responses and/or jerky movement.

Answer 31

• Less / no saltatory conduction; depolarisation occurs along whole length of axon.
  
  • So nerve impulses take longer to reach neuromuscular junction; delay in muscle contraction.
• Ions / depolarisation may pass / leak to other neurones.
  
  • Causing wrong muscle fibres to contract.

Question 32

Describe the factors that affect speed of conductance.

Answer 32

Myelination

• Depolarisation at nodes of Ranvier only resulting in -> saltatory conduction.
• Impulse doesn’t travel / depolarise whole length of axon.

Axon diameter

• Bigger diameter means less resistance to flow of ions in cytoplasm.

Temperature

• Increases rate of diffusion of Na⁺ and K⁺ as more kinetic energy.
• But proteins / enzymes could denature at a certain temperature.

Question 33

Describe the structure of a synapse.

Answer 33

Question 34

What are cholinergic synapses?

Answer 34

• Synapses that use the neurotransmitter acetylcholine (ACh).

Question 35

Describe transmission across a cholinergic synapse.

Answer 35

At pre-synaptic neurone

1. Depolarisation of pre-synaptic membrane causes opening of voltage-gated Ca²⁺ channels.
   
   • Ca²⁺ diffuse into pre-synaptic neurone / knob.
2. Causing vesicles containing ACh to move and fuse with pre-synaptic membrane.
   
   • Releasing ACh into the synaptic cleft (by exocytosis).

At post-synaptic neurone

3. ACh diffuses across synaptic cleft to bind to specific receptors on post-synaptic membrane.
4. Causing Na⁺ channels to open.
   • Na⁺ diffuse into post-synaptic knob causing depolarisation.
   • If threshold is met, an action potential is initiated.

Question 36

Explain what happens to acetylcholine after synaptic transmission.

Answer 36

• It is hydrolysed by acetylcholinesterase.
• Products are reabsorbed by the presynatpic neurone.
• To stop overstimulation - if not removed it would keep binding to receptors, causing depolarisation.

Question 37

Explain how synapses result in unidirectional nerve impulses.

Answer 37

• Neurotransmitter only made in / released from pre-synaptic neurone.
• Receptors only on post-synaptic membrane.

Question 38

Describe summation by synapses.

Answer 38

• Addition of a number of impulses converging on a single post-synaptic neurone.
• Causing rapid build-up of neurotransmitter (NT).
• So threshold more likely to be reached to generate an action potential.

Question 39

Describe spatial summation.

Answer 39

• Many pre-synaptic neurones share one synaptic cleft / post-synaptic neurone.
• Collectively release sufficient neurotransmitter to reach threshold to trigger an action potential.

Question 40

Describe temporal summation.

Answer 40

• One pre-synaptic neurone releases neurotransmitter many times over a short time.
• Sufficient neurotransmitter to reach threshold to trigger an action potential.

Question 41

Describe inhibition by inhibitory synapses

Answer 41

• Inhibitory neurotransmitters hyperpolarise postsynaptic memebrane as:
  
  • Cl⁻ channels open -> Cl⁻ diffuse in.
  • K⁺ channels open -> K⁺ diffuse out.
• This means inside of axon has more negative charge relative to outside / below resting potential.
• So more Na⁺ required to enter for depolorisation,
• Reduces likelihood of threshold being met / action potential formation at post-synaptic membranes.

Question 42

Describe the structure of a neuromuscular junction.

Answer 42

• Very similar to a synapse except:
  
  • Receptors are on muscle fibre sarcolemma instead of postsynaptic membrane and there are more.
  • Muscle fibre forms clefts to store enzyme e.g. acetylcholinesterase to break down neurotransmitter.

Question 43

Compare transmission across cholinergic synapses and neuromuscular junctions.

Answer 43

In both: transmission is unidirectional.
CHOLINERGIC SYNAPSE

• Neurone to neurone (or effectors, glands).
• Neurotransmitters can be excitatory or inhibitory.
• Action potential may be initiated in post-synaptic neurone.

NEUROMUSCULAR JUNCTION

• Motor neurone to muscle.
• Always excitatory.
• Action potential propagates along sarcolemma down T tubules.

Question 44

Use examples to explain the effect of drugs on a synapse.

Answer 44

• Some drugs stimulate the nervous system, leading to more action potentials, e.g.:
  
  • Similar shape to neurotransmitter.
  • Stimulate release of more neurotransmitter.
  • Inhibit enzyme that break downs neurotransmitter -> Na⁺ continues to enter.
• Some drugs inhibit the nervous system, leading to fewer action potentials.
  
  • Inhibit release of neurotransmitter e.g. prevent opening of calcium ion channel.
  • Block receptors by mimicking shape of neurotransmitters.

Question 45

Describe homeostasis.

Answer 45

• Maintenance of a stable internal environemnt within restricted limits.
• By physiological control systems (normally involve negative feedback).
  
  • Examples: core temperature, blood pH, blood glucose concentration & blood water potential.

Question 46

Explain the importance of maintaining stable core temperature.

Answer 46

• If temperature is too high:
  
  • Hydrogen bonds in tertiary structure of enzymes break.
  • Enzymes denature; active sites change shape and substrates can’t bind.
  • So fewer enzyme-substrate complexes.
• If temperature is too low:
  
  • Not enough kinetic energy so fewer enzyme-substrate complexes.

Question 47

Explain the importance of maintaining stable blood pH.

Answer 47

• Above or below optimal pH, ionic / hydrogen bonds in tertiary structure break.
• Enzymes denature; active sites change shape and substractes can’t bind.
• So fewer enzyme substrate complexes.

Question 48

Explain the importance of maintaining stable blood glucose concentration.

Answer 48

Too low (hypoglycaemia)

• Not enough glucose for respiration.
• So less ATP produced.
• Active transport etc. can’t happen -> cell death.

Too high (hyperglycaemia)

• Water potential of blood decreases.
• Water lost from tissue to blood via osmosis.
• Kidneys can’t absorb all glucose -> more water lost in urine causing dehydration.

Question 49

Describe the role of negative feedback in homeostasis.

Answer 49

1. Receptors detect change from optimum.
2. Effectors respond to counteract change.
3. Returning levels to optimum / normal.

• Examples: control of blood glucose concentration, blood pH, core temperature and blood water potential.

Question 50

Explain the importance of conditions being controlled by separate mechanisms involving negative feedback.

Answer 50

• Departures in different directions from the original state can all be controlled / reversed.
• Giving a greater degree of control (over changes in internal environment).

Question 51

Describe positive feedback.

Answer 51

1. Receptors detect changefrom normal.
2. Effectors respond to amplify change.
3. Producing a greater deviation from normal.

• Not involved in homeostasis.
• Examples: onset of contractions in childbirth, blood clotting etc.

Question 52

Describe the structure of a nephron.

Answer 52

• Nephron = basic structural and functional unit of the kidney.
• Associated with each nephron is a network of blood vessels.

Question 53

Summarise the role of different parts of the nephron.

Answer 53

1. **Bowman’s / renal capsule.
   
   • Formation of glomerular filtrate (ultrafiltration).
2. Proximal convoluted tubule.
   
   • Reabsorption of water and glucose (selective reabsorption).
3. Loop of Henle.
   
   • Maintenance of a gradient of sodium ions in the medulla.
4. Distal convoluted tubule & collecting duct.
   
   • Reabsorption of water (permeability controlled by ADH).

Question 54

Describe the formation of glomerular filtrate.

Answer 54

1. High hydrostatic pressure in glomerulus.
   
   • As diameter of afferent arteriole (in) is wider than efferent arteriole (out).
2. Small substances e.g. water, glucose, ions, urea forced into glomerular filtrate, filtered by:
   
   • a. Pores / fenestrations between capillary endothelial cells.
   • b. Capillary basement membrane.
   • c. Podocytes.
3. Large proteins / blood cells remain in blood.

Question 55

Describe the reabsorption of glucose and water by the proximal convoluted tubule.

Answer 55

1. Na⁺ actively transported out of epithelial cells to capillary.
2. Na⁺ moves by facilitated diffusion into epithelial cells down a concentration gradient, bringing glucose against its concentration gradient.
3. Glucose moves into capillary by facilitated diffusion down its concentration gradient.
4. Glucose etc. in capillaries lower water potential.
5. Water moves by osmosis down a water potential gradient.

Question 56

Describe and explain how features of the cells in the PCT allow the rapid reabsorption of glucose into the blood.

Answer 56

• Microvilli / folded cell-surface membrane -> provides a large surface area.
• Many channel / carrier proteins -> for faciliated diffusion / co-transport.
• Many carrier proteins -> for active transport.
• Many mitochondria -> produce ATP for active transport.
• Many ribosomes -> produce carrier / channel proteins.

Question 57

Suggest why glucose is found in the urine of an untreated diabetic person.

Answer 57

• Blood glucose concentration is too high so not all glucose is reabsorped at the PCT.
• As glucose carrier / cotransporter proteins are saturated / working at maximum rate.

Question 58

Explain the importance of maintaining gradient of sodium ions in the medulla (concentration increases further down).

Answer 58

• So water potential decreases down the medulla (compared to filtrate in collecting duct).
• So a water potential gradient is maintained between the collecting duct and medulla.
• To maximise reabsorption of water by osmosis from filtrate.

Question 59

Describe the role of the loop of Henle in maintaining a gradient of sodium ions in the medulla.

Answer 59

1. In the ascending limb:
   
   • Na⁺ actively transported out (so filtrate concentration decreases).
   • Water remains as ascending limb is impermeable to water.
   • This increases concentration of Na⁺ in the medulla, lowering water potential.
2. In the descending limb:
   
   • Water moves out by osmosis then reabsorbed by capillaries (so filtrate concentration increases).
   • Na⁺ ‘recycled’ -> diffuses back in.

Question 60

Suggest why animals needing to conserve water have long loops of Henle (thick medulla).

Answer 60

• More Na⁺ moved out -> Na⁺ gradient is maintained for longer in medulla / higher Na⁺ concentration.
• So water potential gradient is maintained for longer.
• So more water can be reabsorbed from collecting duct by osmosis.

Question 61

Describe the reabsorption of water by the distal convoluted tubule.

Answer 61

• Water moves out of distal convoluted tubule & collecting duct by osmosis down a water potential gradient.
• Controlled by ADH which increases their permeability.

Question 62

What is osmoregulation?

Answer 62

• Control of water potential of the blood (by negative feedback).

Question 63

Describe the role of the hypothalamus in osmoregulation.

Answer 63

1. Contains osmoreceptors which detects increase OR decrease in blood water potential.
2. Produces more ADH when water potential is low OR less ADH when water potential is high.

Question 64

Describe the role of the posterior pituitary gland in osmoregulation.

Answer 64

• Secretes (more / less) ADH into blood due to signals from the hypothalamus.

Question 65

Describe the role of antidiuretic hormone (ADH) when osmoreceptors detect a decrease in blood water potential due to increasing sweating, reduced water intake and increased salt intake.

Answer 65

1. Hypothalamus produces more ADH.
2. Attaches to receptors on collecting duct and distal convoluted tubule.
3. Stimulating addition of channel proteins (aquaporins) into cell-surface membranes.
4. So increases permeability of cells of collecting duct and DCT to water.
5. So increases water re absorption from collecting duct / DCT back into blood by osmosis.
6. So decreases volume and increases concentration of urine produced.

Question 66

Describe the role of antidiuretic hormone (ADH) when osmoreceptors detect a increase in blood water potential.

Answer 66

1. Hypothalamus produces less ADH.
2. Less attaches to receptors on collecting duct and distal convoluted tubule.
3. Less addition of channel proteins (aquaporins) into cell-surface membranes.
4. So low permeability of cells of collecting duct and DCT remain to water.
5. So less water reabsorption from collecting duct / DCT back into blood by osmosis.
6. So increases volume and decreases concentration of urine produced.

Question 67

Describe the factors that influence blood glucose concentration.

Answer 67

• Consumption of carbohydrates -> glucose absorbed into blood.
• Rate of respiration of glucose e.g. increases during exercise due to muscle contraction.

Question 68

Describe the role of the liver in glycogenesis, glycogenolysis and gluconeogenesis.

Answer 68

GLYCOGENESIS

• Converts glucose -> glycogen.

GLYCOGENOLYSIS

• Converts glycogen -> glucose.

GLUCONEOGENESIS

• Converts amino acids and/or glycerol -> glucose.

Question 69

Explain the action of insulin in decreasing blood glucose concentration.

Answer 69

• Beta cells in islets of Langerhans in pancreas detect blood glucose concentration is too high -> secrete insulin:
• Attaches to specific receptors on cell surface membranes of target cells e.g. liver/muscles.

1. This causes more glucose channel proteins to join cell surface membranes of.
   
   • Increasing permeability to glucose.
   • So more glucose can enter cell by facilitated diffusion.
2. This also activates enzymes involved in conversion of glucose to glycogen (glycogenesis).
   
   • Lowering glucose concentration in cells, creating a concentration gradient.
   • So glucose enters cell by facilitated diffusion.

Question 70

Explain the action of glucagon in increasing blood glucose concentration.

Answer 70

• Alpha cells in islets of Langerhans in pancreas detect blood glucose concentration is too low -> secrete glucagon.
• Attaches to specific receptors on cell surface membranes of target cells e.g. liver.

1. Activates enzymes involved in hydrolysis of glycogen to glucose (glycogenolysis).
2. Activates enzymes involved in conversion of glycerol / amino acids to glucose (gluconeogenesis).

• This establishes a concentration gradient -> glucose enters blood by facilitated fissuion.

Question 71

Explain the role of adrenaline in increasing blood glucose concentration.

Answer 71

• Fear / stress/ exercise -> adrenal glands secrete adrenaline.
• Attaches to specific receptors on cell surface membranes of target cells e.g. liver.
• Activates enzymes involved in hydrolysis of glycogen to glucose (glycogenolysis).
• This establishes a concentration gradient -> glucose enters blood by facilitated diffusion.

Question 72

Describe the second messenger model of adrenaline and glucagon action.

Answer 72

• Adrenaline / glucagon (‘first messengers’) attach to specific receptors on cell membrane which:

1. Activates enzyme adenylate cyclase (changes shape).
2. Which converts many ATP to any cyclic AMP (cAMP).
3. cAMP acts as the second messenger -> activates protein kinase enzymes.
4. Protein kinases activate enzymes to break down glycogen to glucose.

Question 73

Suggest an advantage of the second messenger model.

Answer 73

• Amplifies signal from hormone.
• As each hormone can stimulate production of many molecules of second messenger (cAMP).
• Which can in turn activate many enzymes for rapid increase in glucose.

Question 74

Compare the causes of types I and II diabetes.

Answer 74

• Both - higher and uncontrolled blood glucose concentration; higher peaks after meals and remains high.

TYPE I

• Key point = beta cells in islets of Langerhans in pancreas produce insufficient insulin.
• Normally develops in childhood due to autoimmune response destroying beta cells of islets of Langerhans.

TYPE II

• Key point = receptor loses responsiveness / sensitivity to insulin, but insulin still produced.
• So fewer glucose transport proteins -> less uptake of glucose -> less conviction of glucose to glycogen.
• Risk factor = obesity.

Question 75

Describe how type I diabetes can be controlled.

Answer 75

• Injections of insulin (as pancreas doesn’t produce enough).
• Blood glucose concentration monitored with biosensors; dose of insulin matched to glucose intake.
• Eat regularly and control carbohydrate intake e.g. those that broken down / absorbed slower.
  
  • To avoid sudden rise in glucose.

Question 76

Suggest why insulin can’t be taken as a tablet by mouth.

Answer 76

• Insulin is a protein.
• Would be hydrolysed by endopeptidases / exopeptidases.

Question 77

Describe how type II diabetes can be controlled.

Answer 77

• Not normally treated with insulin injections (as pancreas still produces it), but may use drugs which target insulin receptors to increase their sensitivity.
  
  • To increase glucose uptake by cells / tissues.
• Reduce sugar intake (carbohydrates) / low glycaemic index -> less absorbed.
• Reduce fat intake -> less glycerol converted to glucose.
• More (regular) exercise -> uses glucose / fats by increasing respiration.
• Lose weight -> increased sensitivity of receptors to insulin.

Question 78

Describe how you can evaluate the positions of health advisors and the food industry in relation to the increased incidence of type II diabetes.

Answer 78

• Consider both sides:
  
  • Health advisers aim - reduce risk of type II diabetes due to health problems caused.
    
    • So need to reduce obesity as it is a risk factor.
  • Food industry aim - maximise profit.