Usually during childhood or puberty; symptoms develop rapidly
Nutritional status at time of disease onset (Type 1)?
Frequently undernourished
Prevalence (Type 1)?
10% of diagnosed diabetics
Genetic predisposition (Type 1)?
Moderate
Defect or deficiency (Type 1)?
β cells are destroyed, eliminating production of insulin
Frequency of ketosis (Type 1)?
Common
Plasma insulin (Type 1)?
Low to absent
Acute complications (Type 1)?
Ketoacidosis
Response to oral hypoglycemic drugs (Type 1)?
Unresponsive
Treatment (Type 1)?
Insulin is always necessary; either standard (1 or 2 insulin injections daily) or intensive (3 or more insulin injections daily)
Age of onset (Type 2)?
Frequently after age 35; symptoms develop gradually
Nutritional status at time of disease onset (Type 2)?
Obesity usually present
Prevalence (Type 2)?
90% of diagnosed diabetics
Genetic predisposition (Type 2)?
Very strong
Defect or deficiency (Type 2)?
Insulin resistance combined with inability of β cells to produce appropriate quantities of insulin
Frequency of ketosis (Type 2)?
Rare
Plasma insulin (Type 2)?
High early in disease; low in disease of long duration
Acute complications (Type 2)?
Hyperosmolar state
Response to oral hypoglycemic drugs (Type 2)?
Responsive
Treatment (Type 2)?
Diet, exercise, oral hypoglycemic drugs; insulin may or may not be necessary. Reduction of risk factors (smoking cessation, blood pressure control, treatment of dyslipidemia) is essential to therapy.