Morning Hyperglycemic Excursions
A constant failure in the metabolic control of non–insulin-using patients with type 2 diabetes
- Louis Monnier, MD1,
- Claude Colette, PHD2,
- Rémy Rabasa-Lhoret, MD1,
- Hélène Lapinski, MD1,
- Cécile Caubel, MD1,
- Antoine Avignon, MD1 and
- Hélène Boniface, BS1
- 1Department of Metabolic Diseases, Lapeyronie Hospital, Montpellier, France
- 2University Institute of Clinical Research, Montpellier, France
Abstract
OBJECTIVE—To determine whether, over daytime, one or several hyperglycemic excursions exist that can be general failures in the glycemic control of patients with type 2 diabetes.
RESEARCH DESIGN AND METHODS—In 200 non–insulin-using patients with type 2 diabetes, diurnal plasma glucose and insulin profiles were studied. Plasma glucose concentrations were measured after an overnight fast (at 8:00 a.m. immediately before breakfast), during the postprandial period (at 11:00 a.m. and 2:00 p.m.), and during the postabsorptive period (at 5:00 p.m., extended postlunch time).
RESULTS—In the population considered as a whole, prelunch glucose concentrations (12.0 mmol/l) were found to be significantly increased (P < 0.0001) when compared with those observed at 8:00 a.m. (8.8 mmol/l), at 2:00 p.m. (10.5 mmol/l), and at 5:00 p.m. (8.6 mmol/l). Similar significant excursions (P < 0.0001) in prelunch glucose were observed within subsets of patients selected from the following criteria: 1) body weight, 2) HbA1c, 3) categories of treatment, and 4) residual β-cell function. From the calculation of areas under the daytime glucose curves, the relative contributions of postprandial and fasting glucose to the total glucose increment were found to be similar.
CONCLUSIONS—High plasma glucose excursions over morning periods seem to be a permanent failure in non–insulin-using patients with type 2 diabetes, whatever the clinical (BMI), biological (HbA1c), therapeutic, and pathophysiological (residual β-cell function) status. Midmorning glucose testing should be recommended for detecting such abnormalities and for correcting them with appropriate therapies.
Footnotes
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Address correspondence and reprint requests to Professor L. Monnier, Department of Metabolism, Lapeyronie Hospital, 34295 Montpellier Cedex 5, France. E-mail: mal-meta-{at}chu-montpellier.fr.
Received for publication 12 October 2001 and accepted in revised form 27 December 2001.
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