Previously called adult-onset, maturity-onset, or ketosis-resistant diabetes, type II diabetes mellitus involves relative insulin deficiency and resistance to insulin action. The combination of normal or high insulin levels and hyperglycemia implies insulin resistance. Both increased insulin levels and decreased insulin action have been documented in the two groups at increased risk for type II diabetes–the obese and the elderly.
If pancreatic beta-cell reserve is sufficient, hyperinsulinemia preserves normal glucose levels. Eventually, impaired glucose tolerance occurs, although hyperinsulinemia continues. This state of mild glucose intolerance with near-normal fasting blood glucose levels may persist indefinitely. But in patients in whom insulin secretion is subsequently impaired, plasma glucose levels increase to those consistent with diabetes, and plasma insulin levels fall to normal or below. These patients are thought to have an increased genetic susceptibility to decreased beta-cell reserve.
Type II diabetes is distinguished by an absence of ketosis, which indicates that the patient has some effective insulin. About 35% of patients with type II diabetes use exogenous insulin. But unlike patients with type I diabetes, they do not need exogenous insulin to sustain life.
Obesity and age are independent risk factors for type II diabetes mellitus. Some 80% to 90% of type II diabetic patients are obese, and the prevalence doubles for every 20% increase over desirable body weight and for each decade after the fourth, regardless of weight. The prevalence in persons ages 65 to 74 is about 15%. An even higher percentage of people beyond the eighth decade may have type II diabetes mellitus. Type II diabetes is more prevalent in certain populations, eg, American Indians, blacks, and those of Hispanic ancestry.
Secondary Diabetes Mellitus
This category includes diabetes mellitus resulting from diseases that destroy the pancreas (eg, hemochromatosis, pancreatitis, and cystic fibrosis), certain endocrine diseases in which excess hormones interfere with insulin action (eg, growth hormone in acromegaly, cortisol in Cushing’s syndrome, and catecholamines in pheochromocytoma), and certain drugs that suppress insulin secretion (eg, phenytoin) or inhibit insulin action (eg, estrogens or glucocorticoids).
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