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

Kirkman, M. Sue; Shankar, R. Ravi; Shankar, Sudha; Shen, Changyu; Brizendine, Edward; Baron, Alain; McGill, Janet
September 2006
Diabetes Care;Sep2006, Vol. 29 Issue 9, p2095
Academic Journal
OBJECTIVE -- 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 ≥ 200 mg/dl). RESEARCH DESIGN AND METHODS -- 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 ≥ 140 mg/dl). Secondary outcomes included measures of glycemia (meal tolerance tests, HbA1c, 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 β-cell function (HOMA-β, early- and late-phase insulin secretion, and proinsulin-to-insulin ratio). RESULTS -- 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 β-cell function. In a post hoc analysis of subjects with initial FPG <126 mg/dl, acarbose reduced the rate of development of FPG ≥ 126 mg/dl (27 vs. 50%; P = 0.04). CONCLUSIONS -- 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, β-cell failure may no longer be remediable.


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