� Insulin and Glucagon control blood glucose levels in normal

cells.

� Hypoglycaemia – Blood glucose concentration becomes too

low

� Hyperglycaemia – Blood glucose concentration becomes too

high

� Insulin and Glucagon are secreted by cells in the pancreas

known as The Islets of Langerhans.

� α-cells secrete Glucagon

� β-cells secrete Insulin

� Blood glucose levels must be kept in narrow limits;

� After a meal glucose is stored in the form of glycogen in the liver and

skeletal muscle.

� This prevents the blood glucose levels from becoming to high

� The brain requires a constant supply of glucose, so between meals and

overnight, blood glucose levels are maintained by the liver releasing

glucose back into the blood stream.

� This preventing blood glucose from falling to low.

� Diabetes mean “abnormal amount of urine”

� Mellitus comes from Latin meaning “sweet honey”

� An increase in blood glucose concentration (after a meal) stimulates insulin

secretion and decreases glucagon secretion.

� A reduction in blood glucose (between meals) leads to a decrease in insulin

secretion and an increase in glucagon secretion.

� This homeostatic control mechanism is an example of negative feedback control.

� Insulin affects a number of different cell types;

� Skeletal Muscle Cells, Liver Cells and Fat Cells

� Skeletal muscle cells and fat cells have low permeability to

glucose in the absence of insulin.

� Insulin acts by stimulating the uptake of glucose into muscle

and fat cells.

� Cell membranes of liver cells are quite permeable to glucose

� Therefore glucose enters whether or not insulin is present

� However insulin still increases the uptake of glucose by liver

cells and increases glycogen formation.

� Insulin is a protein hormone which binds to a specific

receptors in the cell membrane of its target cells.

� These insulin receptor complexes result in a series of

reactions allowing glucose to pass through the cell

membrane.

� Under certain circumstances (obesity) the insulin receptors

become resistant to the insulin.

� Therefore the glucose uptake of the cell decreases.

� This reduction in the number of receptors leads to insulin

resistance.

� Glucagon when all of the glucose is gone.

� If the body has a low blood sugar concentration the alpha

cells secrete glucagon in order to restore it to its normality.

� Glucagon acts on the liver to increase the breakdown of

glycogen into glucose thus elevating the blood sugar level.

� Insulin-Dependent Diabetes Mellitus (IDDM) is a condition in which the pancreas

ceases to produce enough insulin

� IDDM is caused by the destruction of the insulin producing β-cells in the pancreas

� This results in inadequate insulin production, this commonly occurs in childhood.

� Therefore the glucose present in the blood cannot be absorbed into the cells.

Treatment for Type 1

� Regular injections of insulin

� Insulin cannot be taken orally because it is a protein, as it would be digested by

enzymes in the stomach.

Symptoms

� Fatigue

� Weakness

� Weight loss – caused by the body breaking down fat and protein stores to supply

cells with energy as they cant utilise glucose.

� Non-Insulin Dependent Diabetes Mellitus (NIDDM) is a much more

common disorder (typically after age 40)

� This accounts for thousands of deaths annually worldwide due to an

increased incidence of cardiovascular disease.

� It also causes disability in millions.

� More than 80% of Type 2 diabetics are overweight

� In this condition, individuals can produce insulin, and have insulin levels

in the blood which are normal or higher than normal.

� However the tissues, especially liver and skeletal muscles, become less

sensitive to it.

� This is known as insulin resistance.

� The target cells for insulin appear to have a deficiency of insulin

receptors and this reduces the ability of the skeletal muscle cells

and fat cells to take up glucose.

� The pancreas tries to compensate for this resistance by producing

more insulin.

� This leads to the β-cells in the pancreas becoming “burnt out”.

� Therefore insulin production decreases.

� This results in an increases in blood glucose and diabetes develops.

� At very high levels, the kidneys are unable to absorb all the

glucose passing through them and the excess glucose

appears in the urine.

� Glycosuria – The first stage in the diagnosis of the condition

are from urine tests carried out as part of a routine

examination.

� The excess glucose excreted in the urine carries with it a large

volume of water

� This accounts for the large amount of urine produced

(polyuria).

� Also the subsequent thirst that follows (polydipsia)

� This test is used for the diagnosis of either type of diabetes

mellitus and is based on the fasting individuals response to

drinking the prescribed amount of glucose (50-100g)

dissolved in 1L of water.

� Blood glucose levels are then measured every 30 minutes

over a 2 hour period

� In the diabetic individual fasting blood glucose level tends to

be higher than normal and remains high for several hours.

� In a diabetic person, the blood glucose

concentration does not return to normal as fast as

a non-diabetic person

� The glucose levels also rise considerably more

� It is known that the ability of the cells to uptake

glucose from the blood (insulin sensitivity is greater

in physically fit individuals than in relatively unfit

individuals.

� A decrease in insulin sensitivity with advancing age

can be prevented by regular exercise.

� The adaptation of skeletal muscle as a result of

exercise increases capillary network and blood

flow resulting in;

Exercise-Induced Reduced Insulin Resistance

� This means exercise causes a decrease in insulin

resistance

� This enhances glucose transport due to an increase

in the number of insulin receptors on the muscle

cell membrane.

� Also there is an increase in the enzymes associated

with glucose storage.

� However the improved insulin sensitivity is lost after

5-7 days after the last exercise.

� This is why frequent exercise is important.