Diabetes is
mainly of two types - Diabetes insipidus - a rare form of diabetes
caused by a deficiency of the pituitary hormone vasopressin, which regulates
kidney function that may cause frequent urination & Diabetes mellitus -
caused by impaired formation of insulin by pancreas mainly
due to destruction/decreased responsiveness of islet b-cells.
Diabetes
mellitus is
characterized by the imbalance in the secretion and/or utilization of insulin
which leads to the disorder of carbohydrates (glucose) metabolism in the body.
This results the increase or decrease in the blood glucose. Carbohydrates from
various dietary sources are the primary exogenous source of glucose which is
the main fuel for energy requirement of the body. Therefore, a continuous
supply of glucose is necessary to ensure the proper function and survival of
all organs.
Hence,
mammals have evolved sophisticated systems to maintain the glucose level in the
blood within tight limits, despite large fluctuations in food intake.
Homeostatic mechanisms are in place to maintain blood glucose levels with very
narrow range protecting the body against hypoglycemia during period of fasting
and against the hyperglycemia following the ingestion of a high carbohydrate
diet. These goals are met chiefly through the hormonal modulation of the
production of glucose by the liver and the peripheral uptake of glucose by
skeletal muscle, heart muscle and fat.
When mammals
fast, glucose homeostasis is achieved by triggering expression of gluconeogenic
genes in response to glucagon, and when they take a carbohydrate-rich diet, the
function is taken over by the insulin for its uptake and utilization
peripherally. Defects in carbohydrate metabolizing machinery and consistent
efforts of the physiological system to correct the imbalance in carbohydrate
metabolism place an over-exertion on the endocrine system, which leads to the
deterioration of endocrine control. Continuing deterioration of endocrine
control exacerbates the metabolic disturbances leading primarily to
hyperglycemia and subsequently, the complication thus developed is called
diabetes mellitus.
Type I
diabetes is believed to be an autoimmune disease that results in
specific immunologic destruction of b-cells of islets of Langerhans's,
presence of islet cell antibodies in type I diabetes, lymphocytic infiltration
in and around islets (insulitis) and association of type I diabetes
with other autoimmune diseases supports the evidence of autoimmunity. About 10%
of cases of type I diabetes has other organ specific autoimmune diseases such
as Graves’ disease, Addison’s disease or autoimmune thyroiditis. The another
presentation of insulin-dependent diabetes mellitus has been recently
demonstrated that with immunological testing approximately 10% of patients
initially diagnosed of having non-insulin dependent diabetes mellitus (NIDDM)
may have a slow onset for IDDM that has been termed latent autoimmune diabetes
in adults.
It usually
manifest at early age, generally below the age of 40. The plasma insulin levels
are low and patients respond to exogenous insulin therapy. The onset is marked
by polyurea, polyphagia, and with extreme derangement, ketoacidosis, all
resulting from metabolic dearrangements. A catabolic state is reached because
of insulin deficiency which results in glucose, fat and protein metabolism. Glucose
assimilation in the muscle and liver is greatly reduced and also the stores of
glycogen are depleted by increased glycogenolysis.
This
causes glycosuria. The glycosuria induces osmosis
and thus results in polyurea, causing profound loss of
electrolytes and water. Such a renal water loss and hyperosmolarity causes
depletion of intracellular water provokes the osmoreceptors of the thirst
centers of brain and causes intense thirst i.e. polydipsia. Due to
lack of insulin catabolism of protein and fats occurs resulting in removal of
gluconeogenic amino acid from the liver, this result in negative energy balance
which in turn leads to increasing appetite i.e. polyphagia. Despite
of increased appetite catabolic effect prevails resulting in weight loss and fatigue
but the patients are not obese. Thus type I DM is a classic triad of polyurea,
polydipsia and polyphagia, weight loss and fatigue.
Type II diabetes, or maturity onset diabetes, or non-insulin dependent diabetes mellitus
(NIDDM), is more common and constitutes 80-90% cases of diabetes. The basic
metabolic defect in this type of diabetes is either a delayed insulin secretion
relative to glucose load (deranged insulin secretion), or the peripheral
tissues are unable to respond to insulin (insulin resistance). In this type,
the patient is usually 40 years of age at presentation and 80% are obese.
Ketoacidosis is not a feature but hyperosmolar non-ketotic coma may be a
complication. The pancreas in NIDDM is usually of normal size but with a
tendency to fatty infiltration, most probably due to the obesity present in
many of these patients.
The type II
diabetes is further of two subtypes i.e., obese and non-obese. Obesity is a
common finding in type II diabetes. There is impaired insulin sensitivity of
peripheral tissues, such as muscle and fat cells to the action of insulin, in
obese individuals (insulin resistance). Lack of exercise and obesity are
considered major contributors to type II diabetes; roughly 90% of individuals
with type II diabetes are obese. These conditions predispose to
hyperinsulinemia. Increased insulin resistance results in increased fasting and
postprandial b-cells synthesis, which leads to “b-cell burnout” and
eventually diabetes.
The
condition of insulin resistance may exist for many years before
pancreatic b-cell function actually becomes impaired. Weight reduction in
such obese patients produces improvement in the diabetic state. It has been
observed that insulin resistance is a factor not only in obese type II diabetes
but also in non-obese type II diabetes. In such individuals, the increased
insulin resistance of peripheral tissues is due to either decrease in the
number of insulin receptors or there is post defect.
Gestational
diabetes which refers to the hyperglycemia temporarily during pregnancy in
individuals, having inherited liability to develop this disorder. Although this
form usually disappears following delivery, 40% of women with gestational
diabetes will go on to develop type II diabetes later in life. Other types of
diabetes may be secondary to pancreatic disease or removal of pancreatic
tissue; secondary to endocrine disease such as acromegaly, Cushing’s syndrome, pheochromocytoma,
glucagonoma, somatostatinoma or primary aldosteronism; secondary to
administration of hormones causing hyperglycemia.
Iatrogenic
diabetes may develop during various forms of therapies by drugs such as
antihyperglycemic drugs, thiazide diuretics, preparations containing estrogen,
psychoactive drugs, sympathomimetic agents etc. It is also occurring mainly in
those patients who are genetically susceptible.
The
prevalence of insulin dependent diabetes mellitus (IDDM) is 10% whereas that of
non-insulin dependent diabetes mellitus (NIDDM) is 90% of the diabetic
population. Diabetes mellitus, the most pervasive and costly chronic disease is
afflicted by an estimated 175 million people worldwide. It is a leading cause
of adult blindness and end-stage kidneys disease. Additionally diabetics are
two to four times more likely to have heart disease or to suffer a stroke .
Therefore,
Diabetes mellitus has been recognized as a growing world-wide epidemic by many
health advocacy groups including the World Health Organization (WHO).
Approximately 5% of the world’s population suffers from diabetes. Independent
forecasters have suggested that the global prevalence of the disease will
increase from 150 million in 2000 to 220 million in 2010 and to 300 million by
2025. The global burden of diabetes mellitus would rise from 135.3 in 1995 to
300 million in 2025. The WHO has also estimated that diabetes will be one of
the leading causes of death and disability within the next quarter century.
India being
at top of the world in diabetes cases, known as diabetes capital of the world.
The Indians are more prone to diabetes due to the reason being that Indian
healthcare policies have by and large emphasized on the prevention of
infectious diseases only. Also, with the improved living conditions in India,
we are increasingly following western dietary habits unsuited for our environs,
adopting sedentary life style, and exposed to psycho-social stress. This has
resulted in an unprecedented rise in diabetes population to epidemic
proportions during last few decades in India.
Complications related to
Diabetes mellitus is that the patients with long-standing diabetes may
develop complications affecting the eyes, kidneys or nerves (micro vascular
complications) or major arteries. The major arteries are affected in people
with diabetes, causing a substantial increase in both in coronary artery disease
and strokes as well as peripheral vascular disease. The greatest risk of large
vessel disease occurs in those diabetic patients who develop proteinuria or
micro albuminuria, which are associated with widespread vascular damage.
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