Type 1 : A chronic illness characterized by the body’s inability to produce insulin due to the autoimmune destruction of the beta cells in the pancreas.
Type 2 : An array of dysfunctions characterized by hyperglycemia and resulting from the combination of resistance to insulin action, inadequate insulin secretion, and excessive or inappropriate glucagon secretion.
Type 1 : Autoimmune destruction of the beta cells of the pancreas involves both genetic predisposition and an environmental component.
Complex genetic aspect - multiple genes involved - high sibling relative risk. Dizygotic twins have 5-6% concordance rate - monozygotic twins will share the diagnosis more than 50% of the time by the age of 40.
Those whose mother / father has the disease have a 2 % / 5 % risk.
Potential triggers for immunologically mediated destruction of the beta cells include viruses (eg, enterovirus, mumps, rubella ), toxic chemicals, exposure to cow’s milk in infancy, and cytotoxins.
Type 2 : Presumably, the disease develops when a diabetogenic lifestyle * is superimposed on a susceptible genotype.
*(ie, excessive caloric intake, inadequate caloric expenditure, obesity)
Risk factors for Type 2
Hypertension ( >140/90 ), Dislipidemia (HDL < 40 mg/dl or TGC > 150 rng/dl) Age > 45 , Weight > 120% of desired , first degree family history Hispanic / Native - African - Asian American / Pacific Islander descent.
Previous Impaired Glucose Tolerance / Impaired fasting Glucose Gestational diabetes / delivery of a >4.1 kg baby Polycystic Ovary Syndrome ( which leads to insulin resistance )