Chapter 20 Diabetes Type 2
Non–Insulin Dependent
PATHOPHYSIOLOGY
Type 2 diabetes, previously called non–insulin-dependent diabetes, or adult-onset diabetes, is considered a chronic disease in which hyperglycemia results from insulin deficiency or hyperinsulinemia. Type 2 diabetes is associated with children who are overweight, a positive family history, and insulin resistance. Insulin resistance occurs when fat, muscle, and liver cells resist the insulin molecule both on the cell membrane and inside the cell. This results in the usual enzymatic reaction within the cell. Eventually beta cells are unable to meet the insulin demands of the body. As with Type 1 diabetes, Type 2 leads to hyperglycemia. This occurs as a result of insulin resistance and decreased insulin secretion. The pancreas does not produce enough insulin.
Insulin is necessary for the following physiologic functions: (1) to promote the use and storage of glucose for energy in the liver, muscles, and adipose tissue; (2) to inhibit and stimulate glycogenolysis or gluconeogenesis, depending on the body’s requirements; and (3) to promote the use of fatty acids and ketones in cardiac and skeletal muscles. Insulin deficiency results in unrestricted glucose production without appropriate use, which leads to hyperglycemia and increased lipolysis and production of ketones and, in turn, to lipemia, ketonemia, and ketonuria.
INCIDENCE
1. Girls have a higher prevalence than boys.
2. The onset most commonly occurs around puberty (ages 10–14 years).
3. Type 2 diabetes occurs disproportionately in American Indian, African American, Mexican American, and Pacific Islander youth.
4. Type 2 diabetes accounts for up to half of all diagnosed cases of diabetes in children and adolescents.
