Control of Blood-Glucose Concentration

Question 1

The Action of Insulin.

Answer 1

High blood-glucose concentration.
Detected by receptors on the B-cells of the Islets of Langerhans, causing them to secrete insulin.
Released into blood and travels to liver and muscle cells.
Insuline binds to specific receptors on the cell membrane of the liver or muscle cells.
Liver and muscle cell membrane becomes more permeable to glucose, extra channel proteins are inserted into the membrane.
Glycogenesis. Ezymes are activated that convert glucose to glycogen in the liver and muscle cells.
Glucose is also converted to fats for storage in adipose tissue.
The respiration rate in cells increases.

Question 2

The Action of Glucagon.

Answer 2

Decreased blood-glucose concentration.
Receptors in the Islets of Langerhans detect it and the a-cells secrete glucagon.
Mainly targets liver cells, glucagon bind to specific protein receptors on the cell membrane.
Glycogenolysis. Activates enzymes which catalyse the converstion of glycogen to glucose.
Also stimulates the conversion of amino acids and glycerol to glucose. Gluconeogenesis.

Question 3

The Role of Adrenaline and the Second Messenger Model of Hormone Action.

Answer 3

Adrenaline is secreted from the adrenal gland when blood-glucose concentration is low, during stress and exercise.
It binds to receptors on the cell membrane of liver cells and increases blood-glucose concentration.
Activated enzymes that cause the conversion of glycogen to glucose.
Inactivates an enzyme that synthesised glycogen from glucose.
Both adrenaline and glucagon act via a second messenger.

1. Hormone adrenaline approaches transmembrane protein.
2. Fuses to receptor, causing it to change shape on the inside of the membrane.
3. This activates adenyl cyclase inside the membrane.
4. ATP is converted to cyclic AMP (cAMP)
5. cAMP changes chape and activates protein kinase enzyme.
6. Active protein kinase enzyme catalyses the converstion is glycogen to glucose.

Question 4

Type 1 Diabetes.

Answer 4

Also known as insuline dependent or juvenile onset.
Caused by an inability to produce insulin.
Body’s own immune system may destory B-cells.
Blood-glucose concentration can rise and stay high for a long time after eating, this hyperglycemia can be fatal.
The kidneys cannot absorb all of the extra glucose so some in extreted in the urine..
Treatment: blood-glucose concentrations must be monitored regularly, this can be done using a glucose biosensor.
Insulin can be given by injection.
Balanced diet and exercise to mangage hyperglycemia.

Question 5

Type 2 Diabetes.

Answer 5

Also known as insulin independent and late onset.
Cased by gradual loss in the responsiveness of target cells to insuline do to receptor abnormalities.
Usualy occurs later in life.
Closely linked to obesity. Other risk factors include age, lack of exercise and poor diet.
Treatment: careful regulation of diet, especially sugar intake and balancing this with exercise.
Losing weight is advised.
Eventually, insulin injections may be necessary to control blood glucose concentration.