Ebers (1). The term ‘diabetes’, which is from the Ionian Greek meaning ‘to pass through‘, was first used by Aretaeus of Cappadocia in the second century AD as a generic description of conditions causing increased urine output (2). The association of polyuria with a sweet-tasting substance in the urine was noted in the fifth to sixth century AD by two Indian physicians, Susruta and Charuka (1,2). The urine of certain polyuric patients was described as tasting like honey, sticky to the touch and attracting ants. Two forms of diabetes could be distinguished in the Indians’ descriptions: one affected older, fatter people and the other thin people who did not survive long; this strongly reminds us the present clinical description of Type 2 and Type 1 diabetes.
The term diabetes mellitus, an allusion to the honeyed taste of the urine, was first used in the late
eighteenth century by John Rollo and others (3) to distinguish it from other polyuric states in which
the urine was tasteless. The concept that diabetes was a systemic disease arising in the blood was
elaborated a century before (in the seventeenth century) by Matthew Dobson, a physician in Liverpool (England) who published a series of experiments showing that the serum of a patient
with diabetes, as well as the urine, contained a sweet-tasty substance namely sugar (4). The nineteenth century is the key century that has greatly contributed to the understanding of diabetes. Claude Bernard made numerous discoveries in the field of metabolism and diabetes.
He described the storage of glucose in the liver as a glycogen and the acute hyperglycemia that
followed experimental damage of the medulla oblongata known as ‘piqiire’ diabetes (5). Oskar
Minkowski and Josef Von Mering noted that total pancreatectomy produced diabetes in dogs (6). The pancreatic islets were named after Paul Langerhans by Edouard Lafresse. Langerhans had suggested that pancreatic isfets produced a giucose-lowering substance. This substance was named insulin by Jean de Meyer in 1909, almost a decade before insulin was discovered (7). Although diabetes mellitus has been recognized for many centuries and major advances have been accomplished since the discovery of insulin in the understanding of diabetes and metabolism, there was no clear or widely accepted definition of the diabetic state until the early 80s.
In 1980, the World Health Organization (WHO) Expert Committee on diabetes mellitus (8) defined the diabetic state as a state of chronic hyperglycemia which may result from many environmental and genetic factors often acting jointly.
Hyperglycemia is due to defects in insulin secretion, insulin action or both. This imbalance leads
to disturbances of carbohydrate, fat and protein metabolism. The major effects of diabetes mellitus
include long-term damage, dysfunction and failure of various organs. Diabetes mellitus may present with characteristic symptoms: thirst, polyuria, polydypsia, blurring of vision, weight loss, and infections. In its most severe forms, ketoacidosis or a non-ketotic hyperosmolar state may develop and lead to stupor, coma and, in absence of effective treatment, death. Most of the time, symptoms are not severe, or may be absent, and consequently hyperglyceniia of sufficient degree to cause pathological and functional changes may be present for a long time before the diagnosis is made. The longterm complications of diabetes mellitus include progressive development of disease of the capillaries of the kidney and retina, damage to the peripheral nerves and excessive atherosclerosis.
The clinical manifestations of these complications therefore include nephropathy that may lead to
renal failure, retinopathy with potential blindness, neuropathy with risk of foot ulcers, amputation,
Charcot joints, and features of autonomic dysfunction, including sexual dysfunction.
People with diabetes are at increased risk of cardiovascular, peripheral vascular and cerebrovascular
disease. Diabetes mellitus is thus defined as a set of abnormalities characterized by a state of sustained hypgerglycemia. It is a clinical description with a clienucal definition. Pathogenic mechanisms and various explanations, to be found, lie behind the sustained hyperglycemia. Processes which destroy the beta-cells of the pancreas with consequent insulin deficiency, and others that result in resistance to insulin action are part of a possible group of to insulin action are part of a possible group of processes involved