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Glycemic Variability

Should we and can we prevent it?

¹ Department of Metabolic Diseases, Lapeyronie Hospital, Montpellier, France
² Laboratory of Human Nutrition, University Institute of Clinical Research, Montpellier, France

Address correspondence and reprint requests to Professor Louis Monnier, Department of Metabolic Diseases, Lapeyronie Hospital, 34295 Montpellier Cedex 5, France. E-mail: l-monnier{at}chu-montpellier.fr

Diabetes is characterized by glycemic disorders that include both sustained chronic hyperglycemia and acute glucose fluctuations. There is now cogent evidence for the deleterious effects of sustained chronic hyperglycemia that results in excessive protein glycation and generation of oxidative stress. The role of glucose variability from peaks to nadirs is less documented, but there are many reasons to think that both upward (postprandial) and downward (interprandial) acute fluctuations of glucose around a mean value activate the oxidative stress. As a consequence, it is strongly suggested that a global antidiabetic strategy should be aimed at reducing to a minimum the different components of dysglycemia (i.e., A1C, fasting and postprandial glucose, as well as glucose variability). All the therapeutic agents that act on postprandial glucose excursions seem of particular interest for reducing the latter parameter (i.e., the glucose instability). Particular attention should be paid to such emerging therapeutic agents as the glucagon-like peptide 1 agonists and the dipeptidyl peptidase (DPP)-IV inhibitors that act through the incretin pathway.

Abbreviations: 8-iso-PGF₂, 8-iso-prostaglandin F₂ • MAGE, mean amplitude of glycemic excursions

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