Figure 1. Proposed role of sodium-glucose cotransporter 2 (SGLT2) inhibition in euglycemic diabetic ketoacidosis (eDKA). Classic DKA results from insulin deficiency (absolute or relative) and concurrent increase in counter-regulatory hormones leading to ketosis, hyperglycemia, and osmotic diuresis. In contrast, SGLT2 inhibitor therapy in a well-compensated individual at baseline causes glucosuria, mild volume depletion, and lower serum glucose levels, associated with decreased insulin secretion (green box). During times of intercurrent illness and/or metabolic stress (e.g., surgery or gastrointestinal illness), decreased carbohydrate intake coupled with lower serum glucose levels can further depress insulin secretion. This can ultimately lead to eDKA (red box).
© <2020>. This manuscript version is made available under the CC-BY-NC-ND 4.0 license https://creativecommons.org/licenses/by-nc-nd/4.0
*Possible pathways of carbohydrate deficiency and causes of insulinopenia.
Wang et al. explained this figure [2].
eDKA - euglycemic diabetic ketoacidosis; DKA - diabetic ketoacidosis; SGLT2 - sodium-glucose cotransporter 2; BP - blood pressure; PO - per oral