What you do this lesson

• Copy all notes that appear in blue or green

• Red / White notes are for information and similar notes will be found in your monograph

• Read up on all diabetes information in your monograph for the next lesson

What is Diabetes mellitus?

A failure to control blood glucose levels and an impaired ability to store glucose in the form of liver

and muscle glycogen

Symptoms of diabetes mellitus

Classic symptoms of diabetes are –• Frequent urination, with large volumes of urine (especially at night)• Excessive thirst• Hunger• Weight loss

Other symptoms –• Fatigue• Blurry vision• Gum and urinary tract infections• Slow healing of skin• Genital itching in women

CONTROL OF BLOOD SUGAR LEVELS

• After a meal excess glucose is stored as glycogen in the liver and skeletal muscles)

• As glucose levels fall, the liver releases glucose into the blood stream to prevent hypoglycaemia.

Two hormones control this process -Insulin and Glucagon

Both are secreted in the pancreas by the Islets of Langerhans

Beta (β) cells produce insulin Alpha (a) cells produce glucagon

Control of blood glucose levels by insulin and glucagon

Insulin and its effects

Insulin is a protein hormone which binds to specific receptors on the cell membrane of target cells and initiates the following

• Insulin binds to receptor

• Activated insulin receptor promotes movement of glucose transporter molecules from intracellular pool to the cell membrane

• Glucose transporters allow glucose to enter the cell

• When insulin levels decrease glucose transporters move from cell membrane to intra-cellular storage pool, where they can be recycled

Insulin• Affects skeletal muscle , liver and fat cells and

stimulates the uptake of glucose by these cells

• Insulin increases the permeability of muscles to glucose as normally they are not very permeable

• Liver cells are very permeable but become more so in the presence of insulin and they are also stimulated to increase glycogen formation

In obese individuals the number of insulin receptors decreases and therefore glucose uptake is decreased.

This reduction in receptors leads to insulin resistance

Glucagon

Low blood glucose

Alpha cells of pancreas release glucagon

Liver breaks down glycogen

Glucose released into blood

Complications associated with diabetes –

• Hypertension

• Stroke

• Kidney disease

• Nerve damage

• Increased risk of atherosclerosis

• Impaired vision due to cataracts or damaged retinas.

Diabetic ulceration

Diabetes not controlledproperly may lead to loss of sight through degeneration of retina.

Forms of diabetes mellitus

• Type 1 (early onset, insulin dependent diabetes mellitus

IDDM)

• Type 2 (late onset, non-insulin dependent diabetes mellitus

NIDDM)

Type 1 (IDDM)

• Failure of the pancreas to produce adequate amounts of insulin as a result of an autoimmune response

• Accounts for 5-10% of cases

• The sympton weight loss is caused by body breaking down fat to supply energy as cells cannot utilise glucose

• Treatment = regular insulin injections subcutaneously

Type 2 (NIDDM)

• Accounts for 95% of cases• Associated with obesity• Plasma insulin levels normal but cells are

less sensitive to insulin (insulin resistance)• Reduced uptake of insulin into skeletal

muscle and fat cells• Possibly due to a reduced number of insulin

receptors on the cell membrane

In summary insulin is produced but not used

efficiently by the cells

pancreas compensates by producing more insulin

B cells become “worn out” and insulin production decreases

Blood glucose increases and diabetes develops

For interactive game on diabetes see ‘My Diabetic Dog’At the Nobel Prize medical website

Click here

Treatment for NIDDM

• Diet • Weight control• Adequate exercise• Begin an insulin

increasing agent• Lower blood pressure

Comparison of type 1 and type 2

type 1 type 2

Age under 20 over 40

% of diabetics less than 10% over 90%

appearance of symptoms rapid slow

obesity at onset uncommon common

β cell no. decreased variable

Condition of Cells of Islets inflamed normal

Family history uncommon common