Insulin-sensitive tissues (muscle, liver, and fat) fail to metabolize glucose efficiently in the absence of insulin. In uncontrolled type 1 diabetes, an excess of counter-regulatory hormones (cortisol, catecholamines, and glucagon) contributes to further metabolic dysfunction. In the absence of adequate amounts of insulin, increasing breakdown products of muscle (amino acid proteolysis), fat (fatty acid lipolysis), and glycogen (glucose glycogenolysis) are recognized. There is an increase in glucose production from noncarbohydrate precursors as a result of gluconeogenesis and ketogenesis in the liver. Without prompt treatment, severe metabolic decompensation (i.e., diabetic ketoacidosis) will occur and may lead to death.
Type 2 Diabetes Mellitus Type 2 diabetes mellitus is a heterogeneous form of diabetes that commonly occurs in older age groups (>40 years) and more frequently has a familial tendency than type 1 diabetes. This form of diabetes mellitus accounts for approximately 90% to 95% of those with diabetes. The presence of risk factors strongly inﬂuences the development of type 2 diabetes in susceptible populations.
Risk factors for type 2 diabetes include ethnicity, obesity, family history of DM, sedentary lifestyle, impaired glucose tolerance, upper-body adiposity, and a history of gestational diabetes and hyperinsulinemia.
In contrast to an absence of insulin that occurs with type 1 diabetes, in type 2 diabetes the altered metabolism of insulin results in insulin resistance. This condition is characterized by
Table 9.9 Classification of Diabetes Mellitus 1. Type 1 diabetes
Characterized by pancreatic destruction leading to insulin deficiency
A. Idiopathic
B. Immune mediated 2. Type 2 diabetes
A combination of insulin resistance and some degree of inadequate insulin secretion 3. Other types of diabetes:
A. Impaired glucose tolerance (IGT)
B. Endocrinopathies (Cushing’s, acromegaly, pheochromocytoma, hyperaldosteronism)
C. Drug-or chemical-induced
D. Diseases of the exocrine pancreas (pancreatitis, neoplasia)
E. Infections
F. Genetic defects of beta-cell function and insulin action
G. Gestational diabetes mellitus
Adapted from The Expert Committee on the Diagnosis and Classification of Diabetes Mellitus. Report of the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus. Diabetes Care 2000;23:S4–S42.
impaired glucose uptake in target tissues. A compensatory increase in insulin secretion results, causing higher-than-normal circulating insulin levels (36). Obesity is present in 85% of affected patients. The cause of type 2 diabetes is unknown, but defects in both the secretion and action of insulin are suspected.
Many patients diagnosed with type 2 diabetes at an early age eventually exhaust endogenous pancreatic insulin and require injected insulin. When under severe stress, such as infection or surgery, they may develop diabetic ketoacidosis or a hyperglycemic hyperosmolar nonketotic state.
Diagnosis Three methods are available to diagnose diabetes mellitus in nonpregnant women: 1.
A single fasting blood glucose greater than or equal to 126 mg/dL on two separate occasions 2.
A random blood glucose equal to or above 200 mg/dL in an individual with classic signs and symptoms of diabetes (polydipsia, polyuria, polyphagia, and weight loss) 3.