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| Name | Class |
|---|---|
| American Diabetes Association | OTHER |
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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.
Obese AA patients with a history of DKA who later experience near-normoglycemia remission represent an ideal population in which to define the sequence of events that lead to b-cell dysfunction in type 2 diabetes. The researchers hypothesize that obese AA with DKA will prove particularly susceptible to beta-cells dysfunction due to sustained elevations of plasma glucose (glucose toxicity) and/or free fatty acid levels (lipotoxicity). This study will test beta-cell response by administering a glucose infusion to diabetic African Americans with a history of DKA, diabetic African Americans without a history of DKA, and non-diabetic African Americans.
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| Label | Type | Description | Intervention Names |
|---|---|---|---|
| Participants with ketosis-prone diabetes | Active Comparator | Obese African Americans with type 2 diabetes with history of diabetic ketoacidosis (DKA) receiving Intralipid 20% and a glucose infusion. |
|
| Participants with ketosis-resistant diabetes | Active Comparator | Obese African American with type 2 diabetes with hyperglycemia without ketosis receiving Intralipid 20% and a glucose infusion. |
|
| Non-diabetic control group | Active Comparator | Obese African Americans without diabetes receiving a glucose infusion. |
|
| Name | Type | Description | Arm Group Labels | Other Names |
|---|---|---|---|---|
| Intralipid 20% | Drug | Participants receive a 48-hour infusion with Intralipid at 40 milliliters per hour (mL/hr). |
|
| Measure | Description | Time Frame |
|---|---|---|
| First-Phase Insulin Release (FPIR) | An arginine stimulation test was used to evaluate beta-cell function and insulin secretion. Increased glucose in the blood causes insulin to be released, beginning with a spike in insulin in the first 10 minutes and plateauing 2 to 3 later. Diminished first-phase insulin release is an early indicator of beta-cell dysfunction. Two sequential arginine stimulation tests were performed, the first set before and the second after completion of the 20-hour dextrose infusion. The first-phase insulin release (FPIR) was calculated as the sum of the insulin levels at 2, 3, 4, and 5 minutes after the arginine infusion. FPIR is expected to rise after the dextrose (glucose) infusion and FPIR generally rises less in persons with impaired glucose tolerance. | Hour 0, Hour 20 |
| Measure | Description | Time Frame |
|---|---|---|
| Number of Participants With Beta-cell Failure | Pancreatic beta-cells can adapt to insulin resistance during the early stages of diabetes but continuous exposure of beta-cells to prolonged hyperglycemia can cause irreversible damage due to glucotoxicity. This study aimed to evaluate whether hyperglycemia-induced reduced beta-cell failure was the result of beta-cell exhaustion or beta-cell desensitization, however, no participants experienced beta-cell failure so this original analysis could not be performed. |
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Inclusion Criteria:
Exclusion Criteria:
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| Name | Affiliation | Role |
|---|---|---|
| Guillermo Umpierrez, MD | Emory University | Principal Investigator |
| Facility | Status | City | State | ZIP | Country | Contacts |
|---|---|---|---|---|---|---|
| Grady Memorial Hospital | Atlanta | Georgia | 30303 | United States |
| PubMed Identifier | Type | Citation | Retractions |
|---|---|---|---|
| 20067967 | Result | Gosmanov AR, Smiley D, Robalino G, Siqueira JM, Peng L, Kitabchi AE, Umpierrez GE. Effects of intravenous glucose load on insulin secretion in patients with ketosis-prone diabetes during near-normoglycemia remission. Diabetes Care. 2010 Apr;33(4):854-60. doi: 10.2337/dc09-1687. Epub 2010 Jan 12. |
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Participant enrollment began in March 2004 and all study follow-up was completed in December 2009. The study was conducted at the Clinical Research Center at Grady Memorial Hospital in Atlanta, Georgia.
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| ID | Title | Description |
|---|---|---|
| FG000 | Ketosis-prone Diabetics | Obese African Americans with type 2 diabetes and a history of diabetic ketoacidosis (DKA) receiving a 48-hour infusion of Intralipid 20% at 40 mL/hour and a glucose infusion of 10% dextrose infused at a rate of 200 mg/m^2/min for 20 hours. |
| FG001 | Ketosis-resistant Diabetics | Obese African Americans with type 2 diabetes with hyperglycemia without ketosis receiving a 48-hour infusion of Intralipid 20% at 40 mL/hour and a glucose infusion of 10% dextrose infused at a rate of 200 mg/m^2/min for 20 hours. |
| FG002 | Non-diabetic Control Group | Obese African Americans without diabetes receiving a glucose infusion of 10% dextrose infused at a rate of 200 mg/m^2/min for 20 hours. |
| Title | Milestones | Reasons Not Completed | ||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| Overall Study |
|
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| ID | Title | Description |
|---|---|---|
| BG000 | Ketosis-prone Diabetics | Obese African Americans with type 2 diabetes and a history of diabetic ketoacidosis (DKA) receiving a 48-hour infusion of Intralipid 20% at 40 mL/hour and a glucose infusion of 10% dextrose infused at a rate of 200 mg/m^2/min for 20 hours. |
| BG001 | Ketosis-resistant Diabetics |
| Units | Counts |
|---|---|
| Participants |
|
| Title | Description | Population Description | Parameter Type | Dispersion Type | Unit of Measure | Calculate Percentage | Denominator Units Selected | Denominators | Classes |
|---|---|---|---|---|---|---|---|---|---|
| Age, Continuous | Mean |
| Type | Title | Description | Population Description | Reporting Status | Anticipated Posting Date | Parameter Type | Dispersion Type | Unit of Measure | Calculate Percentage | Time Frame | Units Analyzed | Denominator Units Selected | Arm/Group Information | Denominators | Classes | Analyses | |||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| Primary | First-Phase Insulin Release (FPIR) | An arginine stimulation test was used to evaluate beta-cell function and insulin secretion. Increased glucose in the blood causes insulin to be released, beginning with a spike in insulin in the first 10 minutes and plateauing 2 to 3 later. Diminished first-phase insulin release is an early indicator of beta-cell dysfunction. Two sequential arginine stimulation tests were performed, the first set before and the second after completion of the 20-hour dextrose infusion. The first-phase insulin release (FPIR) was calculated as the sum of the insulin levels at 2, 3, 4, and 5 minutes after the arginine infusion. FPIR is expected to rise after the dextrose (glucose) infusion and FPIR generally rises less in persons with impaired glucose tolerance. | Posted | Mean | Standard Deviation | microunits/ml | Hour 0, Hour 20 |
|
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| ID | Title | Description | Deaths (Affected) | Deaths (At Risk) | Serious Events (Affected) | Serious Events (At Risk) | Other Events (Affected) | Other Events (At Risk) |
|---|---|---|---|---|---|---|---|---|
| EG000 | Ketosis-prone Diabetics | Obese African Americans with type 2 diabetes and a history of diabetic ketoacidosis (DKA) receiving a 48-hour infusion of Intralipid 20% at 40 mL/hour and a glucose infusion of 10% dextrose infused at a rate of 200 mg/m^2/min for 20 hours. |
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| Term | Organ System | Source Vocabulary | Assessment Type | Notes | Statistical Information |
|---|---|---|---|---|---|
| hyperglycemia | Endocrine disorders | Systematic Assessment | blood sugar intermittently > 300 |
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| Title | Organization | Phone | Extension | |
|---|---|---|---|---|
| Guillermo Umpierrez | Emory University | 404-778-1665 | geumpie@emory.edu |
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| ID | Term |
|---|---|
| D003924 | Diabetes Mellitus, Type 2 |
| D006943 | Hyperglycemia |
| ID | Term |
|---|---|
| D003920 | Diabetes Mellitus |
| D044882 | Glucose Metabolism Disorders |
| D008659 | Metabolic Diseases |
| D009750 | Nutritional and Metabolic Diseases |
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| Glucose infusion | Drug | Participants receive a glucose infusion consisting of 10% dextrose infused intravenously at a rate of 200 mg/m^2/min for 20 hours. |
|
| Hour 20 |
Obese African Americans with type 2 diabetes with hyperglycemia without ketosis receiving a 48-hour infusion of Intralipid 20% at 40 mL/hour and a glucose infusion of 10% dextrose infused at a rate of 200 mg/m^2/min for 20 hours. |
| BG002 | Non-diabetic Control Group | Obese African Americans without diabetes receiving a glucose infusion of 10% dextrose infused at a rate of 200 mg/m^2/min for 20 hours. |
| BG003 | Total | Total of all reporting groups |
| years |
|
| Sex: Female, Male | Count of Participants | Participants |
|
| Race (NIH/OMB) | Count of Participants | Participants |
|
| Region of Enrollment | Count of Participants | Participants |
|
| OG001 | Ketosis-resistant Diabetics | Obese African Americans with type 2 diabetes with hyperglycemia without ketosis receiving a 48-hour infusion of Intralipid 20% at 40 mL/hour and a glucose infusion of 10% dextrose infused at a rate of 200 mg/m^2/min for 20 hours. |
| OG002 | Non-diabetic Control Group | Obese African Americans without diabetes receiving a glucose infusion of 10% dextrose infused at a rate of 200 mg/m^2/min for 20 hours. |
|
|
| Secondary | Number of Participants With Beta-cell Failure | Pancreatic beta-cells can adapt to insulin resistance during the early stages of diabetes but continuous exposure of beta-cells to prolonged hyperglycemia can cause irreversible damage due to glucotoxicity. This study aimed to evaluate whether hyperglycemia-induced reduced beta-cell failure was the result of beta-cell exhaustion or beta-cell desensitization, however, no participants experienced beta-cell failure so this original analysis could not be performed. | Posted | Count of Participants | Participants | Hour 20 |
|
|
|
| 0 |
| 8 |
| 0 |
| 8 |
| 1 |
| 8 |
| EG001 | Ketosis-resistant Diabetics | Obese African Americans with type 2 diabetes with hyperglycemia without ketosis receiving a 48-hour infusion of Intralipid 20% at 40 mL/hour and a glucose infusion of 10% dextrose infused at a rate of 200 mg/m^2/min for 20 hours. | 0 | 7 | 0 | 7 | 1 | 7 |
| EG002 | Non-diabetic Control Group | Obese African Americans without diabetes receiving a glucose infusion of 10% dextrose infused at a rate of 200 mg/m^2/min for 20 hours. | 0 | 13 | 0 | 13 | 0 | 13 |
|
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| D004700 | Endocrine System Diseases |