Control of blood glucose concentration

Where is blood glucose concentration monitored?

• Pancreas

Glycogenolysis

• Hydrolysis of glycogen to release glucose which diffuses into the blood

Gluconeogenesis

• Formation of glucose from non-carbohydrate sources including glycerol and amino acids

Glycogenesis

• Formation of glycogen from alpha glucose

If glucose levels too high?

• Beta cells in islets of Langerhans

• Secrete insulin

How does insulin reduce levels of glucose?

• Increase the rate of respiration

• Increase amount of glucose absorbed into body cells

• Stimulate enzymes of the liver to polymerise glucose into glycogen - glycogenesis

Insulin action

• Binds to receptors on the cell surface membrane of target cells (liver cells)

• Causes vesicle with Glut 4 channel protein to migrate to membrane and fuse with it

• Channel protein inserted into plasm membrane

• Increased facilitated diffusion of glucose out of blood, into cells

Insulin second messenger system

• Activates enzymes to convert glucose to glycogen (glycogenesis)

• Maintains concentration gradient of glucose so diffusion continues

If glucose levels too low?

• Alpha cells of pancreas

• Secrete Glucagon

• Acts on liver

How does glucagon increase glucose levels?

• Stimulates glycogenolysis (glycogen → glucose)

• Stimulates gluconeogenesis (non-carbohydrate sources → glucose)

Role of adrenaline

• Increases heart rate, bp

• Increases blood glucose concentrations to support increased respiration

• Stimulates glycogenolysis

• Inhibits glycogenesis

• Also acts on pancreas to inhibit insulin secretion + stimulate glucagon

Glucagon (and adrenaline) second-messenger model

• Bind to specific receptor on the cell membrane

• Causes a change in shape which activates adenylate cyclase

• Adenylate cyclase converts ATP to cyclic AMP (second messenger)

• cAMP stimulates a cascade of protein kinases

• Produces activated enzymes

Cause of type I diabetes

• Immune system attacking the Islets of Langerhans in the pancreas

• Beta cells that produce insulin are destroyed

• The person no longer produces insulin

Onset of type I

• Diagnosed in childhood

• Rapid onset

Treatment of type I

• Life-long, regular intramuscular injections og insulin

• Insulin pump

Hypoglycaemia

• Too much insulin (not enough exercise or food)

• Blood glucose concentration too low

• Coma

Cause of type II diabetes

• Unhealthy diet (high sugar)

• Lack of exercise

Onset of type II

• Middle-aged and older people

• Can occur in younger children if they are obese

• Family history increases risk: genetic factors

• Slow onset (pre-diabetes - raised but not high enough)

Insulin resistance

• In type II, pancreas produces insulin

• Receptors on cells in the liver + muscles do not respond to it

Treatment for type II

• Increased exercise

• Healthier diet

• Drugs such as metformin which helps insulin work more effectively

• Advanced cases (not controlled with diet/drugs) patient may inject insulin