Types Of Diabetes

Types of diabetes:-

1-Type 1 diabetes (previously insulin dependent diabetes) is:

due to B-cell destruction, usually leading to absolute insulin
deficiency). It can be immune mediated or idiopathic.

2-Type 2 diabetes (previously non-insulin dependent
diabetes)

 ranges from those with predominant insulin
resistance associated with relative insulin deficiency, to those
with a predominantly insulin secretory defect with insulin
resistance.

Type 1 and Type 2 diabetes are the commonest forms of
primary diabetes mellitus. The division is important both
clinically in assessing the need for treatment, and also in
understanding the causes of diabetes which are entirely
different in the two groups.
 
Type 1 diabetes
 
Type 1 diabetes is due to destruction of B-cells in the
pancreatic islets of Langerhans with resulting loss of insulin
production. 

A combination of environmental and genetic
factors that trigger an autoimmune attack on the B-cells is
responsible, occurring in genetically susceptible individuals.
 
Thus, among monozygotic identical twins only about one-third
of the pairs are concordant for diabetes in contrast to the
situation in Type 2 diabetes where almost all pairs are
concordant. 

The process of islet destruction probably begins
very early in life and is known to start several years before the
clinical onset of diabetes.


HLA status

The major histocompatibility complex antigens are adjuncts
to several types of immunological activity. Ninety percent of
Type 1 diabetic patients show either DR3 or DR4, or both
together, while DR2 is protective against diabetes.
 
Autoantibodies and cellular immunity
Islet cell antibodies are present at diagnosis in most Type 1
diabetic patients and gradually decline and disappear during
the following years. 

Antibodies to specific proteins have more
recently been identified: these include antibodies to glutamic
acid decarboxylase (GAD, a 64-kDa antigen); and even closer
association is found in the presence of antibodies to tyrosine
phosphatase (37 kDa, IA-2). 

The presence in a non-diabetic
individual of three or more antibodies (islet cell antibodies,
anti-GAD antibodies, anti-IA-2 antibodies, anti-insulin
autoantibodies) indicates an 88% chance of developing
diabetes within 10 years.
 
The presence of insulinitis at the onset of Type 1 diabetes
represents the role of inflammatory cells (for example, cytotoxic
T cells and macrophages) in B-cell destruction.

Macrophages
also produce cytokines leading to activation of lymphocytes
known to be present at the onset of Type 1 diabetes.
 
Attempts have been made to prevent the onset of Type 1
diabetes. Immune suppression can to some extent preserve islet
function, but permanent remissions are not normally achieved
and the treatment is in any case too dangerous for routine use

The use of nicotinamide to prevent diabetes by altering
macrophage function has not proved to be of benefit. Giving
insulin itself may conserve islet function; the results of trials
are awaited.
 
Associated autoimmune disorders
The incidence of coeliac disease, Addison’s disease,
hypothyroidism, and pernicious anaemia are increased in
Type 1 diabetic patients, and appear to occur especially in
those with persisting islet cell antibodies.
 
Risks of inheriting diabetes
A child of a mother with Type 1 diabetes has an increased risk
of developing the same type of diabetes, amounting to
1-2% by 25 years; the risk is about three times greater if the
father has this disease. If both parents have the disease the risk
is further increased and genetic counselling should be sought
by these rare couples.
 

Type 2 diabetes
There are numerous causes of Type 2 diabetes, which is now
known to include a wide range of disorders with differing
progression and outlook. 

The underlying mechanism is due
either to diminished insulin secretion—that is, an islet defect,
associated with increased peripheral resistance to the action of
insulin resulting in decreased peripheral glucose uptake, or
increased hepatic glucose output. Probably as many as 98% of
 
Type 2 diabetic patients are “idiopathic”—that is, no specific
causative defect has been identified. 

Whether decreasing insulin
secretion or increasing insulin resistance occurs first is still
uncertain, but the sequence of events may vary in different
individuals. 
Obesity is the commonest cause of insulin
resistance. Other rare insulin resistant states are shown in
the table.
 
Some adults (especially those not overweight) over 25 years
of age who appear to present with Type 2 diabetes may have
latent autoimmune diabetes of adulthood (LADA) and become
insulin dependent. Autoantibodies are often present in this
group of patients.
 
Type 2 diabetes is a slowly progressive disease: insulin
secretion declines over several decades, resulting in an
insidious deterioration of glycaemic control which becomes
increasingly difficult to achieve.

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