3.6.4.2 Control of blood glucose concentration

Question 1

Glycogenesis

Answer 1

Formation of glycogen from glucose

Question 2

Glycogenolysis

Answer 2

breakdown of glycogen to glucose

Question 3

Gluconeogenesis

Answer 3

formation of NEW glucose from non carbohydrates

Question 4

Response when blood glucose is too high

Answer 4

• Insulin releases by beta cells in the Islets of Langerhans in the pancreas into the blood
• Insulin travels to effectors liver and muscle cells and bind to receptors on cell surface membrane
• It increases the permeability of target cells to glucose by increasing the number of channel proteins to increase rate of facilitated diffusion of glucose into target cells down concentration gradient
• Insulin also activates enzymes that catalyse glycogenesis
• stimulates lipid formation from glucose
• Insulin increases rate of respiration in muscle cells so more glucose is used - less glucose in cell, increases gradient, increases rate of F.D.

Question 5

Response when blood glucose is too low

Answer 5

• Glucagon secreted by alpha cells in Islets of Langerhans into the blood, where it travels to liver effector cells and binds to receptors
• This activates enzymes in the liver to catalyse glycogenolysis and gluconeogenesis
• Glucagon reduces the rate of respiration in liver cells

Question 6

Effect of adrenaline

Answer 6

• released from adrenal glands during stress or exercise
• increases glucose
• binds to receptors on liver cells
• activates glycogenolysis (glucagon secretion)
• inhibits glycogenesis (inhibits insulin secretion and ability to bind to receptors)

Question 7

What does a second messenger do?

Answer 7

Amplifies the signal (internal signal)

Activates enzymes for glycogenolysis

• Adrenaline and glucagon act via a second messenger cAMP

Question 8

Stages of second messenger model

Answer 8

1. Adrenaline binds to complementary receptors on cell membrane
2. This activates adenylate cyclase
3. Adenylate cyclase converts ATP into cAMP
4. cAMP activates protein kinase A
5. Protein kinase A activates a chain of reactions - glycogenolysis

no cAMP - no glycogenolysis nor gluconeogenesis

Question 9

Type 1 diabetes

Answer 9

• Insulin not produced
• Genetic - gene must be triggered
• Autoimmune - antibodies produced by plasma cells destroy insulin producing beta cells
• Treated with insulin therapy

Question 10

Type 2 diabetes

Answer 10

• may produce less insulin but most display lower sensitivity of target receptors to insulin
• Can be reversed
• Insulin injections usually ineffective as this won’t alter receptors
• Treated with diet and exercise

Question 11

How is glucose reabsorbed?

Answer 11

1. Sodium pumped out of the proximal convoluted tubule cell using the Na+/K+ pump
2. This reduces the [Na+] in the cell, creating a Na+ concentration gradient
3. Na+ is drawn into the cell by the PCT down its concentration gradient, it moves through a co-transport protein with glucose
4. Glucose moves out of the cell by facilitated diffusion into the capillaries

Question 12

What affects the rate of glucose absorption?

Answer 12

• required transport proteins
• the number of transport proteins is a limiting factor
• if there is a higher than normal glucose concentration in the filtrate it cannot all be absorbed and is lost in the urine

Question 13

How does urea change?

Answer 13

• concentration of urea increases due to loss of water from filtrate
• but the amount (mol) of urea doesn’t change as it isn’t reabsorbed

Question 14

How do concentrations of glucose, urea and salt ions change as distance increases across PCT?

Answer 14

• Glucose - ALL of the glucose leaves the glomerular filtrate by co transport
• Salt - most of the salts leave the filtrate by active transport and facilitated diffusion
• Urea - concentration increases due to the loss of water from the filtrate into the blood, but the amount of urea doesn’t change as it is not reabsorbed