This handout provides a general over-view of the topics covered and is not
intended to provide a comprehensive list. Further reading around the topics
covered is encouraged.

• On clinical grounds, patients can be divided into type-1 and type-2 diabetes,
although some subjects are difficult to classify.

• A history of ketoacidosis provides evidence for type-1 diabetes and insulin
treatment is mandatory.

• The concept of type-1 and type-2 diabetes not only encompasses clinical
aspects but also includes aetiological and pathological mechanisms.

Type-1 diabetes:

• HLA associated (HLA-DR3 and DR4)

• Islet cell antibodies

• 30-50% concordance in identical twins

• Viruses and toxins have been suspected as environmental agents involved in
the atiology of type-1 diabetes

• There is a pre-diabetic period, then gradual decline in beta-cell function.
When insulin production is reduced to 10% of normal diabetes may appear.
This may then be followed by the 'honeymoon period'.

• Incidence of type-1 diabetes varies in different countries, it is highest in
northern Europe, being commoner with increasing latitude.

• This may imply a genetic predisposition in northern european populations or
may be the effect of local environmental antigens.

• The incidence of type-1 diabetes is increasing particularly in children < 5
years.

Type-2 diabetes:

• HLA unrelated

• No islet cell antibodies

• Nearly 100% concordance in identical twins

• The prevalence of type-2 diabetes varies in different populations. It is
particularly high in certain communities such as the Pima Indians in Arizona
and the Pacific Islands. This may be due to genetic factors, or intra-uterine
nutrition (The thrifty genotype).

• Type-2 diabetes is 4 times more prevalent in people of Asian and Afro-
Caribbean origin.

The incidence of type-2 diabetes is set to double by the year 2010.

• There is a strong association between type-2 diabetes and obesity.

• There is a combination of insulin resistance and beta-cell dysfunction

• Numerous defects at the level of the insulin receptor have been identified.

Treatment of diabetes:

Type-1:

• Diet plus insulin

• All patients are reviewed by a dietician on a regular basis

• There should be a detailed assessment of the patients eating habits, taking
into account lifestyle, work patterns and culture.

• Each patient requires an individually tailored diet plan.

• Dietary fibre is increased and there should be a reduction in saturated fat
intake.

• Easily absorbed refined carbohydrate should be avoided

• Alcohol in moderation.

Type-2:

• The importance of diet and exercise can not be stressed enough.

• Overweight patients should be advised to loose weight.

• Patients should be set a target BMI (body mass index), calculated by dividing
the weight in kg by the height in meters squared.

• Oral hypoglycaemic agents should be prescribed only when diet has failed
and not as a substitute for diet.

• Oral agents used are sulphonylureas, biguinides (metformin), alpha-
glucosidase inhibitors. Newer insulin-sensitisers (thiozolidinediones) will be
available in a years time.

• The treatment of type-2 diabetes not only involves treatment of blood-glucose
but attention must be paid to other cardiovascular risk factors in addition to
obesity, such as hypertension, dyslipidaemia and smoking. Cardiovascular
disease is the main cause of morbidity and mortality in type-2 diabetes.

Monitoring of glycaemic control and diabetic complications:

• All diabetic patients should perform home monitoring of glycaemic control,
preferably in the form of blood glucose monitoring

• The measurement of HbAlc (glycosylated haemoglobin) provides an estimate
of longer term control (3 months)

• There is a strong correlation between microvascular complications of diabetes
(retinopathy, neuropathy and nephropathy) and high HbAlc

• Patients should aim for as low HbAlc as possible avoiding frequent
hypoglycaemic attacks.