Scientific article
Open access

Impact of SGLT Inhibitors on Multiple Organ Defects in Diabetes

Published inCurrent diabetes reviews, vol. 16, no. 5, p. 411-418
Publication date2020-05-12

Introduction: Diabetes leads to multiple organ defects and cellular dysfunctions such as increased expression of sodium-glucose like transporters (SGLTs). These transporters contribute to glucose homeostasis through glucose reabsorption in the proximal renal tubule. When inhibited, it results in reduced hyperglycemia, increased glucosuria and decreased HbA1c.

Aims: This review article summarizes the positive and adverse effects of the three main SGLT inhibitors used in Europe, on different organs with the aim of providing useful information to clinicians in order to select the adapted SGLT inhibitor in regard to patient health problems.

Discussion: Recently, SGLT pharmacological inhibitors have been developed to manage hyperglycemia in diabetic patients. SGLT inhibitors like canagliflozin, dapagliflozin, empagliflozin were approved by the Food and Drug Administration (FDA) in 2013 for use in Europe. Beyond their impact on glucose re-uptake by the kidney, these inhibitors exert beneficial pleiotropic effects. Nevertheless, several studies have recently warned the scientific community regarding adverse effects of these agents. Therefore, clinicians should consider these effects to adapt the treatment regarding patients' health.

Conclusion: The use of SGLT inhibitor in the treatment of type 2 diabetes should be considered with the perspective of general health state of the patient. In fact, SGLT inhibitors promote pleiotropic effects, among which some are beneficial for certain organs while some are deleterious.

  • Canagliflozin
  • Chronic diseases
  • Dapagliflozin
  • Diabetes
  • Empagliflozin
  • Sodium glucose-cotransporter.
Citation (ISO format)
ASRIH, Mohamed, GARIANI, Karim. Impact of SGLT Inhibitors on Multiple Organ Defects in Diabetes. In: Current diabetes reviews, 2020, vol. 16, n° 5, p. 411–418. doi: 10.2174/1573399815666191105151828
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Article (Published version)
ISSN of the journal1573-3998

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