No abstract

2016-11-02T18:49:00

Long-term use of metformin in DPPOS was associated with biochemical B12 deficiency and anemia. Routine testing of vitamin B12 levels in metformin-treated patients should be considered.

We have learned much in the past 10 years about how to help patients to acquire diabetes-related knowledge and skills and how to use strategies to help patients change behaviors. However, the application of knowledge and techniques should be guided by a relevant, coherent, educational philosophy. Empowerment offers a practical conceptual framework for diabetes patient education. Empowering patients provides them with the knowledge, skills, and responsibility to effect change and has the potential to promote overall health and maximize the use of available resources. It is an idea whose time has come for diabetes education.

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 b-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 b-cells cannot secrete sufficient insulin to compensate for insulin resistance, abnormalities in glucose homeostasis ensue, potentially progressing to prediabetes and type 2 diabetes as b-cell function deteriorates further (2-9). The relationship between b-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 b-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 b-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 firstand second-phase insulin secretion, resulting in ;85% lower DI (2). Additional abnormalities in youth with type 2 diabetes include impaired glucose sensitivity of insulin secretion, lower serum adiponectin concentrations, and reduced incretin effect (3,9-13). While upregulation of a-cell function with hyperglucagonemia has been implicated in the pathophysiology of type 2 diabetes in adults (14,15), there are limited data in youth with type 2 diabetes, with studies showing either hyperglucagonemia or no difference from control subjects without diabetes (3,11,16,17). Cross-sectional and longitudinal studies in youth with obesity along the spectrum of glycemia from normoglycemia to prediabetes to type 2 diabetes show, as in adults, that b-cell failure with declining insulin secretion relative to insulin sensitivity results in prediabetes and type 2 diabetes in high-risk youth (5-9,18-21). Importantly, however, prior to reaching the American Diabetes Association (...