|“The discussion and the argument have been about the possibility that the moderate rise in ketonemia that is observed in patients once they go on an SGLT2 inhibitor may be responsible for these metabolic changes by making available beta-hydroxybutyrate—a “super fuel”—because it can be taken up freely by both the kidney and the heart, and it is not insulin dependent. It can be utilized as a substrate to produce energy in a very efficient way; by efficient, one means using less oxygen for the same amount of adenosine triphosphate (ATP) produced, or conversely, using the same amount of oxygen to produce more ATP, to then be invested in contractility.?”|
|The SLGTi is inhibiting effects of insulin, as shown by inhibition of glucose and sodium reabsorption in kidneys and enabling of ketogenesis, as well as lowering blood glucose. These effects, not a specific effect of ketones per se, may be the factor reversing CVD.