PATHOPHYSIOLOGY The progression toward T2DM is influenced by both genetic and lifestyle risk factors that lead to insulin resistance and eventual pancreatic β-cell dysfunction. While aerobic exercise increases insulin sensitivity, a diet high in carbohydrates and fat increases the demand for insulin. So a sedentary lifestyle, combined with a high-carbohydrate, high-fat diet, gradually results in a state of insulin resistance. Compensatory hyperinsulinism will maintain normoglycemia for an indeterminate amount of time; but eventually, pancreatic “burnout” leads to pancreatic β-cell dysfunction and decreased insulin secretion. Relative insulin deficiency then causes decreased cellular glucose uptake, hyperglycemia, and ultimately, T2DM.11
Additional pathophysiologic deficiencies and malfunctions that contribute to hyperglycemia include increased glucagon secretion, decreased incretin effect, and increased renal glucose reabsorption.12
CLINICAL PRESENTATION Clinical presentation of T2DM varies greatly among pediatric patients. Classic symptoms may include polydipsia and polyuria related to hyperglycemia. In addition, the patient or his/her family may note frequent infections or visual disturbances (eg, blurred or diminished vision). However, particularly in the pediatric population, the patient is often asymptomatic.13
On examination, the clinician may observe that the child or adolescent is overweight or obese. He or she may have mild to severe acanthosis nigricans on the posterior neck, axillae, abdomen, or thighs and over the antecubital fossa. However, acanthosis nigricans may not manifest in patients with fairer skin. In severe cases, patients with T2DM may present with hyperglycemic hyperosmolar nonketotic coma or diabetic ketoacidosis.14
