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A review of the mechanism of action, metabolic profile and haemodynamic effects of sodium‐glucose co‐transporter‐2 inhibitors
Author(s) -
Brown Emily,
Rajeev Surya P.,
Cuthbertson Daniel J.,
Wilding John P. H.
Publication year - 2019
Publication title -
diabetes, obesity and metabolism
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.445
H-Index - 128
eISSN - 1463-1326
pISSN - 1462-8902
DOI - 10.1111/dom.13650
Subject(s) - type 2 diabetes , diabetes mellitus , medicine , diabetic ketoacidosis , transporter , blood pressure , glucose transporter , endocrinology , ketoacidosis , pharmacology , mechanism (biology) , chemistry , insulin , type 1 diabetes , biochemistry , philosophy , epistemology , gene
Inhibition of glucose transport in the kidney, to produce glucosuria and thus directly lower blood glucose seems a remarkably simple way to treat diabetes (type 1 or type 2). The development of sodium‐glucose co‐transporter‐2 (SGLT2) inhibitors and their subsequent clinical development has on one hand shown this to be true, but at another level has helped reveal a complex web of interacting effects starting in the kidney and modulating multiple metabolic pathways in a variety of other organs. These underlie the now clear benefits of this class of drugs in the management of type 2 diabetes from glucose lowering, weight loss and blood pressure reduction through to the reductions in cardiovascular and renal complications observed in long‐term outcomes trials. They also explain some of the adverse effects that have emerged, including the risk of diabetic ketoacidosis. This review describes the effects of SGLT2 inhibition in relation to this complex physiology, and shows how this can favourably alter the pathophysiology of type 2 diabetes.