Diabetes mellitus is a greatly challenging disease of the 21 century, and the 
mortality rate due to this insidious disease is increasing worldwide in spite of 
availability of effective oral hypoglycemic agents. Satisfactory management of 
glycemic control in patients afflicted with type 2 diabetes mellitus (T2DM) 
remains a major clinical challenge. Identification of potential pharmacological 
target sites is therefore continuing as an integral part of the diabetic 
research. The sodium-glucose co-transporter type 2 (SGLT2) expressed in the 
renal proximal tubule plays an essential role in glucose reabsorption. 
Pharmacological blockade of SGLT2 prevents glucose reabsorption and subsequently 
induces the elimination of filtered glucose via urine, the process is known as 
'glucuresis'. Dapagliflozin is a selective inhibitor of SGLT2. The US FDA 
approved dapagliflozin in January 2014 to improve glycemic control along with 
diet and exercise in adult patients afflicted with T2DM. It has a potential to 
decrease glycated hemoglobin and to promote weight loss. Although the mechanism 
of action of dapagliflozin is not directly linked with insulin or insulin 
sensitivity, reduction of plasma glucose by dapagliflozin via induction of 
glucosuria could improve muscle insulin sensitivity. Moreover, dapagliflozin 
could cause diuresis and subsequently fall in blood pressure. In addition to 
general discussion on the pharmacology of dapagliflozin, we propose in this 
review the possibilities of dual antidiabetic effect of dapagliflozin and its 
possible additional beneficial actions in hypertensive-obese-T2DM patients 
through its indirect blood pressure-lowering action and reduction of body 
calories and weight. Long-term clinical studies are however needed to clarify 
this contention.