Treating postprandial hyperglycemia does not appear to delay progression of early type 2 diabetes

The Early Diabetes Intervention Program

M. Sue Kirkman, R. Ravi Shankar, Sudha Shankar, Changyu Shen, Edward Brizendine, Alain Baron, Janet McGill

Research output: Contribution to journalArticle

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Abstract

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.

Original languageEnglish
Pages (from-to)2095-2101
Number of pages7
JournalDiabetes Care
Volume29
Issue number9
DOIs
StatePublished - 2006

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Acarbose
Hyperglycemia
Type 2 Diabetes Mellitus
Fasting
Glucose
Insulin Resistance
Glucose Tolerance Test
Homeostasis
Placebos
Insulin
Proinsulin
Survival Analysis
Meals
Research Design
Outcome Assessment (Health Care)

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism

Cite this

Kirkman, M. S., Shankar, R. R., Shankar, S., Shen, C., Brizendine, E., Baron, A., & McGill, J. (2006). Treating postprandial hyperglycemia does not appear to delay progression of early type 2 diabetes: The Early Diabetes Intervention Program. Diabetes Care, 29(9), 2095-2101. https://doi.org/10.2337/dc06-0061

Treating postprandial hyperglycemia does not appear to delay progression of early type 2 diabetes : The Early Diabetes Intervention Program. / Kirkman, M. Sue; Shankar, R. Ravi; Shankar, Sudha; Shen, Changyu; Brizendine, Edward; Baron, Alain; McGill, Janet.

In: Diabetes Care, Vol. 29, No. 9, 2006, p. 2095-2101.

Research output: Contribution to journalArticle

Kirkman, MS, Shankar, RR, Shankar, S, Shen, C, Brizendine, E, Baron, A & McGill, J 2006, 'Treating postprandial hyperglycemia does not appear to delay progression of early type 2 diabetes: The Early Diabetes Intervention Program', Diabetes Care, vol. 29, no. 9, pp. 2095-2101. https://doi.org/10.2337/dc06-0061
Kirkman, M. Sue ; Shankar, R. Ravi ; Shankar, Sudha ; Shen, Changyu ; Brizendine, Edward ; Baron, Alain ; McGill, Janet. / Treating postprandial hyperglycemia does not appear to delay progression of early type 2 diabetes : The Early Diabetes Intervention Program. In: Diabetes Care. 2006 ; Vol. 29, No. 9. pp. 2095-2101.
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N2 - 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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