Treating Postprandial Hyperglycemia Does Not Appear to Delay Progression of Early Type 2 Diabetes The Early Diabetes Intervention Program

Indiana University School of Medicine, 545 Barnhill Dr., EH 421, Indianapolis, IN 46202, USA.
Diabetes Care (Impact Factor: 8.42). 10/2006; 29(9):2095-101. DOI: 10.2337/dc06-0061
Source: PubMed


Postprandial hyperglycemia characterizes early type 2 diabetes. We investigated whether ameliorating postprandial hyperglycemia with acarbose would prevent or delay progression of diabetes, defined as progression to frank fasting hyperglycemia, in subjects with early diabetes (fasting plasma glucose [FPG] <140 mg/dl and 2-h plasma glucose > or =200 mg/dl).
Two hundred nineteen subjects with early diabetes were randomly assigned to 100 mg acarbose t.i.d. or identical placebo and followed for 5 years or until they reached the primary outcome (two consecutive quarterly FPG measurements of > or =140 mg/dl). Secondary outcomes included measures of glycemia (meal tolerance tests, HbA(1c), annual oral glucose tolerance tests [OGTTs]), measures of insulin resistance (homeostasis model assessment [HOMA] of insulin resistance and insulin sensitivity index from hyperglycemic clamps), and secondary measures of beta-cell function (HOMA-beta, early- and late-phase insulin secretion, and proinsulin-to-insulin ratio).
Acarbose significantly reduced postprandial hyperglycemia. However, there was no difference in the cumulative rate of frank fasting hyperglycemia (29% with acarbose and 34% with placebo; P = 0.65 for survival analysis). There were no significant differences between groups in OGTT values, measures of insulin resistance, or secondary measures of beta-cell function. In a post hoc analysis of subjects with initial FPG <126 mg/dl, acarbose reduced the rate of development of FPG > or =126 mg/dl (27 vs. 50%; P = 0.04).
Ameliorating postprandial hyperglycemia did not appear to delay progression of early type 2 diabetes. Factors other than postprandial hyperglycemia may be greater determinants of progression of diabetes. Alternatively, once FPG exceeds 126 mg/dl, beta-cell failure may no longer be remediable.

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    • "Insulin resistance has been recognized as the key factor in the development of type 2 diabetes [5–7]. Moreover, data from clinical trials have shown that IR can be reduced by weight loss and changes in lifestyle behaviors and that early interventions to reduce IR can delay or prevent the onset of type 2 diabetes [8–12]. Thus, there is a need to identify individuals with IR before they develop glucose intolerance and type 2 diabetes; various methods are available, but the practical diagnosis of IR remains a challenge. "
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