The Potential Cardioprotective Mechanism of Sodium-Glucose Cotransporter 2 Inhibitors
- Author:
Jae Han JEON
1
Author Information
- Publication Type:Original Article
- Keywords: Cardiovascular diseases; Diabetes mellitus; Ketones; Sodium-glucose transport proteins
- MeSH: Adipose Tissue; Cardiovascular Diseases; Diabetes Mellitus; Diuresis; Heart; Heart Failure; Hemodynamics; Inflammation; Insulin Resistance; Ketones; Natriuresis; Oxidative Stress; Sodium-Glucose Transport Proteins
- From:Journal of Korean Diabetes 2019;20(2):81-86
- CountryRepublic of Korea
- Language:Korean
- Abstract: The potential mechanism by which sodium-glucose cotransporter 2 (SGLT2) inhibitors prevent cardiovascular disease (CVD) is being widely investigated. Improved insulin resistance, along with decreased body fat mass associated with SGLT2 inhibitor treatment is consistent with previously well-established factors contributing to the prevention of CVD. These factors are responsible for reduction of oxidative stress as well as improvement of systemic inflammation. Because heart failure was one of the most dramatically improved cardiovascular events in various clinical trials and because SGLT2 inhibitors promote osmotic diuresis and natriuresis, hemodynamic changes are considered as a critical mechanism responsible for the cardioprotective effect of SGLT2 inhibitors. Restored tubuloglomerular feedback by SGLT2 inhibitors might play a role in renoprotection, which in turn, leads to fewer CVDs. Finally, blood ketone body increments in response to SGLT2 inhibition might act as a “super-fuel” for salvaging the failing diabetic heart.
