Mechanism Underlying Beta-cell Failure in Obese African Americans With History of Hyperglycemic Crises

• Status: Completed
• Trial end date: 2009-12-01
• Target enrollment: 0
• Participant gender: All

Summary

Obesity is common in African American (AA) patients with newly diagnosed diabetes who present with diabetic ketoacidosis (DKA). Despite the presentation with severe symptoms of insulinopenia and ketoacidosis, clinical and immunogenetic observations indicate that most obese AA patients with DKA have type 2 diabetes. In such patients, previous studies reveal that: a) at presentation, obese AA patients with DKA have markedly decreased pancreatic insulin secretion, lower than in obese non-DKA patients admitted with comparable hyperglycemia, but significantly greater than in lean patients with DKA; b) aggressive diabetic management results in significant improvement in beta-cell function and insulin sensitivity sufficient to allow discontinuation of insulin therapy within 3 months of follow-up. Based on these observations the researchers conclude that similar to obese patients with hyperglycemia, most obese AA with DKA have type 2 diabetes, and that although defects in both insulin secretion and insulin action are present, transient b-cell failure is the primary defect in the development of ketoacidosis.

• Phase: N/A
• Accepts Healthy Volunteers?: Accepts Healthy Volunteers

Details

• Lead Sponsor: Emory University
• Collaborator: American Diabetes Association
• Treatments: Soybean oil, phospholipid emulsion

Criteria

Inclusion Criteria:

• Obese African American subjects (body mass index (BMI) equal or greater than 30)

• Age 18-65

• Patients with a history of diabetic ketoacidosis as defined by the American Diabetes Association (ADA) criteria

• Patients admitted with hyperglycemia but without ketoacidosis (blood glucose greater than 400ml/dl without evidence of ketosis/ketones

• Obese nondiabetic controls (BMI >30; ruled out for diabetes with a 75g oral glucose tolerance test)

Exclusion Criteria:

• Patients with positive autoimmune markers (islet cell or glutamic acid decarboxylase (GAD) autoantibodies)

• Patients with significant medical or surgical illness, including but not limited to myocardial ischemia, congestive heart failure, chronic renal insufficiency, liver failure, and infectious processes

• Patients with recognized or suspected endocrine disorders associated with increased insulin resistance, such as hypercortisolism, acromegaly, or hyperthyroidism

• Patients with bleeding disorders, thrombocytopenia, or abnormalities in coagulation studies

• Patients with fasting hyperglycemia (blood glucose > 120 mg/dl) after discontinuation of insulin therapy

• Pregnancy