Evaluation and Management of Youth-Onset Type 2 Diabetes: A Position Statement by the American Diabetes Association
- Silva Arslanian1,2⇑,
- Fida Bacha3,
- Margaret Grey4,5,
- Marsha D. Marcus6,
- Neil H. White7 and
- Philip Zeitler8
- 1Division of Pediatric Endocrinology, Metabolism, and Diabetes Mellitus, University of Pittsburgh, Pittsburgh, PA
- 2Center for Pediatric Research in Obesity and Metabolism, UPMC Children’s Hospital of Pittsburgh, Pittsburgh, PA
- 3Children’s Nutrition Research Center, Texas Children’s Hospital and Baylor College of Medicine, Houston, TX
- 4Yale School of Nursing, New Haven, CT
- 5Yale School of Medicine, New Haven, CT
- 6University of Pittsburgh School of Medicine, Pittsburgh, PA
- 7Washington University School of Medicine in St. Louis, St. Louis, MO
- 8Children’s Hospital Colorado and University of Colorado School of Medicine, Aurora, CO
- Corresponding author: Silva Arslanian, silva.arslanian{at}chp.edu.
INTRODUCTION
Although all types of diabetes result in hyperglycemia, the pathophysiology of each type of diabetes is different. These guidelines summarize available data specific to the comprehensive care of youth with type 2 diabetes. The objective is to enrich the recognition of type 2 diabetes in youth, its risk factors, its pathophysiology, its management, and the prevention of associated complications.
PATHOPHYSIOLOGY
Glucose homeostasis is maintained by a balance between insulin secretion from the pancreatic β-cells and sensitivity to insulin in skeletal muscle, adipose tissue, and liver (1). When insulin sensitivity declines, insulin secretion must increase to maintain glucose tolerance, and, in most youth, decreased insulin sensitivity due to puberty and/or obesity is compensated by increased insulin secretion. However, when β-cells cannot secrete sufficient insulin to compensate for insulin resistance, abnormalities in glucose homeostasis ensue, potentially progressing to prediabetes and type 2 diabetes as β-cell function deteriorates further (2–9). The relationship between β-cell function and insulin sensitivity in adults and youth has been demonstrated to be a hyperbolic function and can be described mathematically as the product of insulin sensitivity and β-cell function, called the disposition index (DI) (1). The DI essentially expresses the amount of insulin being secreted relative to the degree of insulin resistance and is a constant for a given degree of glucose tolerance in any one individual.
Overweight and obesity are major acquired contributors to the development of insulin resistance, particularly in the face of the physiologic insulin resistance characteristic of puberty. Robust pancreatic β-cell compensatory insulin secretion maintains normal glucose homeostasis. However, in adolescents with obesity who develop type 2 diabetes, there is severe peripheral and hepatic insulin resistance, with ∼50% lower peripheral insulin sensitivity than peers with obesity without diabetes, along with increased fasting hepatic glucose production and inadequate first- and second-phase insulin secretion, resulting …