Classification

Today the designation type I DM, or insulin­dependent diabetes, has replaced terms such as ketosis-prone, juvenile-onset, brittle, and so forth, whereas type II DM, or non-insulin-dependent dia­betes, has replaced the terms ketosis-resistant, maturity-onset, and mild diabetes.

Approximately 90 to 95 percent of all individuals with DM may be classified as non-insulin-depen- dent, and about 5 percent as classically insulin­dependent. Diabetes may also be secondary to certain conditions or syndromes that result in the permanent or temporary destruction of the insulin-producing pancreatic islet cells. Some 2 percent of diabetes have DM secondary to disease, genetic syndromes, drugs, chemicals, or traumatic injury.

History of the CIassiGcation

As early as the sixth century, Hindu physicians rec­ognized the clinical symptoms of diabetes and attrib­uted them to dietary indiscretion. Early descriptions were based on the classic symptoms of diabetes, in­cluding its most salient sign of excessive urination. The term diabetes, meaning “to run through,” was first used in the second century by Aretaeus.

In 1679 Tli ^ιmas Willis noted the sweet taste of urine from diabetics, and in 1776 Matthew Dobson of Manchester was able to demonstrate that one could assay the amount of sugar in the urine by evaporating it and weighing the dried residue. Dob­son stated that this residue looked and tasted like “ground sugar.” It was by the absence of this sweet taste that DM was distinguished from diabetes in­sipidus.

From the mid-1700s until the 1970s, many types of diabetes were described. Observations by Apolli­naire Bouchardat, culminating in his 1875 book on glycosuria, clearly distinguished two types of diabe­tes: In type I, the patients were relatively young; the onset was acute, weight loss was striking, and death ensued rapidly from ketoacidosis — the buildup of poi­sonous ketones from excessive fat metabolism. In type II, the patients were older and tended to be overweight, and the onset was slower. Some of these individuals could control their glycosuria with a low carbohydrate diet.

Much of the early work focused on elucidating the causes of polyuria. John Rollo, in the late 1790s, did an extended metabolic study of an obese diabetic patient at the Greenwich Naval Hospital. He noted that the amount of urine excreted depended upon the type of food that was eaten. Urinary production increased after ingestion of vegetables and de­creased when the diet was high in animal fat and protein. These findings shifted the focus from the kidneys to the gastrointestinal tract and provided a scientific basis for therapeutic diets high in fat and protein and low in carbohydrates.

The gross autopsies that were performed in the 1850s and 1860s revealed no abnormalities of the pancreas of diabetics. In 1855 the French physiolo­gist Claude Bernard discovered that the liver se­cretes glucose from the “animal starch” stored in it. Bernard and Moritz Schiff, furthermore, found that the apparent destruction of the pancreas in experi­mental animals did not result in the onset of diabe­tes.

Specialized “heaps of cells” had been identified in the pancreas by Paul Langerhans in 1869. Contin­ued research by Minkowski and others in the 1890s demonstrated that these “islets of Langerhans” were the source of an “internal secretion” that regulated glycosuria. This work suggested convincingly that DM is caused by a disorder of the endocrine portion of the pancreas. In 1921 Charles Best and Frederick Banting (Toronto) were able to isolate the internal secretion and named it insulin. They realized that insulin is responsible for the control of blood glucose levels and the appearance of clinical symptoms asso­ciated with diabetes. During the 1920s, other hor­monal secretions of the pituitary and adrenals were discovered, which indicated that glucose control is more complex. However, insulin alone constituted the antidiabetes hormone used in therapy.

Although insulin was first used in 1922, it was not until the 1950s that appropriate bioassays of human insulin were developed. These definitive measure­ments clearly showed that individuals with juvenile­onset, or type I, diabetes produced no insulin at all, whereas individuals with maturity-onset, or type II, diabetes had varying amounts of insulin produced by the pancreas. This discovery provided a clear ratio­nale for insulin therapy in those individuals with type I DM, and for diet, exercise, and, after 1955, oral hypoglycemic agents in those with type II diabetes.

The first major epidemiological study of DM, by Haven Emerson and Louise D. Larimore (1924), at­tempted to explain the increases in diabetes mortal­ity in New York City from 1866 to 1923. A number of factors were considered influential, including race, affluence, lack of physical activity, and changes in dietary habits, which emphasized the increasing abundance of all foods. These authors also noted an increasing prevalence of DM among females over the age of 45. It is, however, the famous American diabetologist Elliott P. Joslin whose studies in the 1930s concerning the “epidemic” of diabetes (Joslin, Dublin, and Marks 1933; Joslin 1935) demonstrated the utility of the epidemiological approach.