Overview of Sodium-Glucose Co-Transport Inhibitors

It has been almost 100 years since the discovery of a substance produced by the pancreas, which was named insulin. Now known to be the key regulator of blood glucose homeostasis, the impact this has had on diabetic patients has resulted in increased lifespan and decreased disease complications. Since the discovery of the role of the pancreas and insulin in the pathophysiology of diabetes, researchers have developed a number of drug classes aimed at increasing insulin secretion from the beta cells of the pancreas, increasing insulin sensitivity of target organs, and decreasing glucose production by the liver. With all of the treatment options for type 2 diabetic patients, it's curious as to why large portions of this disease population do not reach or maintain their goal blood glucose levels. Researchers continue to develop and test new medications with different pharmacologic activity in hopes of finding a solution to this problem. The newest addition to the oral anti-diabetic medications, sodium-glucose cotransport (SGLT2) inhibitors, acts independently of insulin to increase glucose excretion from the body [1]. These medications have shown a lot of promise in the treatment of diabetic patients by proven efficacy in reducing HbA1c and with a minimal side effect profile. With any new class of medications, safety profile is a concern and drug companies are required to do post-marketing studies to identify any possible adverse reactions. The FDA issued a warning in May 2015, indicating a possible association between SGLT2 inhibitors and ketoacidosis. These cases warrant further review of the pharmacologic relationship with this metabolic state.