Diabetes Mellitus (DM)

The term diabetes is derived from a Greek word meaning “going through” and mellitus from the Latin word for
“honey” or “sweet.”
Diabetes is a metabolic disorder. It is a disorder of carbohydrate, protein, and fat metabolism resulting from an
imbalance between insulin availability and insulin need. It can represent an absolute insulin deficiency,
impaired release of insulin by the pancreatic beta cells, inadequate or defective insulin receptors, or the
production of inactive insulin or insulin that is destroyed before it can carry out its action. A person with
uncontrolled diabetes is unable to transport glucose into fat and muscle cells; as a result, the body cells are
starved, and the breakdown of fat and protein is increased.
Classification of DM
Type 1 Diabetes Mellitus
Type 1 diabetes mellitus is characterized by destruction of the pancreatic beta cells.8 Type 1 diabetes is
subdivided into two types: type 1A, immune-mediated diabetes, and type 1B, idiopathic diabetes. In the United
States and Europe, approximately 10% of people with diabetes mellitus have type 1 diabetes, with 95% of them
having type 1A, immune-mediated diabetes. Type 1A diabetes is characterized by autoimmune destruction of
beta cells. This type of diabetes, formerly called juvenile diabetes, occurs more commonly in young persons
exogenous insulin replacement to reverse the catabolic state, control blood glucose levels, and prevent ketosis.
The rate of beta cell destruction is quite variable, being rapid in some individuals and slow in others. The
rapidly progressive form commonly is observed in children, but also may occur in adults.
It has been suggested that type 1A, immune-mediated diabetes results from a genetic predisposition (i.e.,
diabetogenic genes), a hypothetical triggering event that involves an environmental agent that incites an
immune response, and immunologically mediated beta cell destruction. Much evidence has focused on the
inherited major histocompatibility complex (MHC) genes that encode three human leukocyte antigens (HLA-
DP, HLA-DQ, and HLA-DR) found on the surface of body cells.
Type 1 diabetes–associated autoantibodies may exist for years before the onset of hyperglycemia. There are two
major types of autoantibodies: insulin autoantibodies (IAAs), and islet cell autoantibodies and antibodies
directed at other islet autoantigens, including glutamic acid decarboxylase (GAD).

Type 2 Diabetes Mellitus and the Metabolic Syndrome

Type 2 diabetes mellitus is a heterogeneous condition that describes the presence of hyperglycemia in
association with relative insulin deficiency. In contrast to type 1 diabetes in which absolute insulin deficiency is
present, type 2 diabetes can be associated with high, normal, or low insulin levels. However, in the presence of
insulin resistance, the insulin cannot function effectively, and hyperglycemia can result. Type 2 diabetes is
therefore a disorder of both insulin levels (beta cell dysfunction) and insulin function (insulin resistance).12
Type 2 diabetes (unlike type 1) is not associated with HLA markers or autoantibodies. Most people with type 2
diabetes are older and overweight; however, type 2 diabetes is becoming a more common occurrence in obese
adolescents.13,14 The metabolic abnormalities that contribute to hyperglycemia in people with type 2 diabetes
include (1) impaired beta cell function and insulin secretion, (2) peripheral insulin resistance, and (3) increased
hepatic glucose production.12 Insulin resistance initially produces an increase in beta cell secretion of insulin
(resulting in hyperinsulinemia as the body attempts to maintain a normoglycemic state. In time, however, the
insulin response declines because of increasing beta cell dysfunction. This results initially in elevated
postprandial blood glucose levels. Eventually, fasting blood glucose levels also rise until frank type 2 diabetes
occurs. During the evolutionary phase, an individual with type 2 diabetes may eventually develop absolute
insulin deficiency because of progressive beta cell failure. As with persons with type 1 diabetes, these persons
require insulin therapy to survive. Because most persons with type 2 diabetes do not have an absolute insulin
deficiency, they are less prone to develop ketoacidosis as compared with people with type 1 diabetes (the
presence of circulating insulin in most type 2 diabetics suppresses ketone body formation).