Diabetes mellitus refers to a group of conditions characterized by high levels of blood glucose,
commonly referred to as blood sugar.
During digestion, carbohydrates in food are broken down into glucose which is carried
by the bloodstream to various organs of the body.
Glucose is taken up by the cells and is either consumed as an energy source or stored for
later use.
Insulin is a hormone produced by beta cells of the pancreas and is necessary for driving
glucose into cells.
Binding of insulin to its receptor on target cells triggers a signaling cascade that brings
glucose transporters to the cell membrane.
When insulin is deficient, glucose cannot enter the cells; it stays in the blood, causing
high blood sugar levels while the cells are deprived of nutrition.
This results in unexplained weight loss and increased hunger.
As blood sugar level exceeds the ability of the kidneys to reabsorb, it overflows into
urine, taking water along with it, resulting in large volumes of urine, dehydration and
excessive thirst.
In the long run, too much sugar in the blood may cause damages to blood vessels, resulting
in increased risks of cardiovascular diseases such as heart attack and stroke.
Damaged vessels in the eyes may lead to loss of vision; while in the kidneys, renal failure
may result.
High blood sugar is also toxic to the nerves, resulting in numbness, tingling and reduced
pain perception.
This, together with impaired wound healing can lead to development of skin ulcers, most
commonly in the feet.
Acute hyperglycemic crises may develop when diabetic patients undergo additional stress
such as infections, other illness or inadequate treatment.
These complications involve severe disturbances of blood homeostasis and are potentially life-threatening.
There are two major types of diabetes mellitus.
In type 1, beta cells of the pancreas are destroyed by the body’s own immune system
by mistake.
The exact mechanism remains unclear, but genetic factors are believed to play a major role,
with at least 50 genes involved in predisposition to the disease.
Insulin production is reduced; less insulin binds to its receptor on target cells; less
glucose is taken into the cells; more glucose stays in the blood.
Type 1 is characterized by early onset, symptoms usually start suddenly, before the age of
20.
Type 1 diabetes is “insulin dependent” and can be successfully managed with insulin
replacement.
In type 2 diabetes, the pancreas produces enough insulin but something goes wrong either
with receptor binding or the signaling cascade in the target cells.
The cells are not responsive to insulin and therefore cannot import glucose.
Type 2 diabetics are said to be “insulin resistant”.
Here again, genetic factors predispose susceptibility to the disease, but lifestyle plays a major
role.
Type 2 is characterized by adult onset; symptoms appear gradually, usually after the age of
30.
Management focuses on weight loss and includes a low-carb diet.