Impact des inhibiteurs du cotransporteur sodium-glucose de type 2 (SGLT2) sur la glycémie post-prandiale

Postprandial glucose excursions contribute to the overall hyperglycemia in persons with type 2 diabetes. This contribution is particularly marked in those who exhibit a satisfactory glycemic control (HbA1c<7.5 %). In most persons with type 2 diabetes, SGLT2 inhibitors lower to 100mg/dl the glycemic threshold for the appearance of glucose in urine and thus result in a downward translation of 24-h glycemic profiles with parallel improvements in both basal glucose (at fasting and interprandial time points) and prandial glucose excursions. In those who have a « residual dysglycemia » (HbA1c between 6.5 and 7.0 %) basal glucose values remain within the near normal range (around 100mg/dl) and glucose disorders are predominantly in the form of abnormal postmeal glucose excursions. In such a situation, sodium-glucose cotransporter 2 (SGLT2) inhibitors target their action on postprandial glucose whereas basal glucose values remain unchanged. An increased efficacy on postprandial glucose might be obtained from a concomitant suppression of SGLT2 and SGLT1 since the latter is expressed both in the gut and the kidney, whilst the former is only present in the renal tubule. However it is highly likely that such a suppression might result in adverse events that would impair the clinical use of these inhibitors. At the present time, the best option seems to favor the development of medications specifically addressed to SGLT2 inhibition, despite limitations in their overall efficacy on HbA1c (from -0.5 to -0.8 %) and uncertainties in their action on postprandial glucose.