The DOI matches its Crossref record; 15 of the 15 references it cites were found in a registry or an index.
SGLT2 Inhibitors May Predispose to Ketoacidosis
Open accessAbstract
CONTEXT: Sodium glucose cotransporter 2 (SGLT2) inhibitors are antidiabetic drugs that increase urinary excretion of glucose, thereby improving glycemic control and promoting weight loss. Since approval of the first-in-class drug in 2013, data have emerged suggesting that these drugs increase the risk of diabetic ketoacidosis. In May 2015, the Food and Drug Administration issued a warning that SGLT2 inhibitors may lead to ketoacidosis. EVIDENCE ACQUISITION: Using PubMed and Google, we conducted Boolean searches including terms related to ketone bodies or ketoacidosis with terms for SGLT2 inhibitors or phlorizin. Priority was assigned to publications that shed light on molecular mechanisms whereby SGLT2 inhibitors could affect ketone body metabolism. EVIDENCE SYNTHESIS: SGLT2 inhibitors trigger multiple mechanisms that could predispose to diabetic ketoacidosis. When SGLT2 inhibitors are combined with insulin, it is often necessary to decrease the insulin dose to avoid hypoglycemia. The lower dose of insulin may be insufficient to suppress lipolysis and ketogenesis. Furthermore, SGLT2 is expressed in pancreatic α-cells, and SGLT2 inhibitors promote glucagon secretion. Finally, phlorizin, a nonselective inhibitor of SGLT family transporters decreases urinary excretion of ketone bodies. A decrease in the renal clearance of ketone bodies could also increase the plasma ketone body levels. CONCLUSIONS: Based on the physiology of SGLT2 and the pharmacology of SGLT2 inhibitors, there are several biologically plausible mechanisms whereby this class of drugs has the potential to increase the risk of developing diabetic ketoacidosis. Future research should be directed toward identifying which patients are at greatest risk for this side effect and also to optimizing pharmacotherapy to minimize the risk to patients.
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Metabolic response to sodium-glucose cotransporter 2 inhibition in type 2 diabetic patients
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Dapagliflozin improves muscle insulin sensitivity but enhances endogenous glucose production
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Glucagon Regulates Hepatic Kisspeptin to Impair Insulin Secretion
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Cited by
Heerspink, H. J. L., Perkins, B. A., Fitchett, D. H., Husain, M., & Cherney, D. Z. I. (2016) · Circulation · doi:10.1161/circulationaha.116.021887 · Cited by 1,376
Diabetic emergencies - ketoacidosis, hyperglycaemic hyperosmolar state and hypoglycaemia
Umpierrez, G., & Korytkowski, M. (2016) · Nature Reviews Endocrinology · doi:10.1038/nrendo.2016.15 · Cited by 563
Dhatariya, K. K., Glaser, N. S., Codner, E., & Umpierrez, G. E. (2020) · Nature Reviews Disease Primers · doi:10.1038/s41572-020-0165-1 · Cited by 461
Effects of sotagliflozin added to insulin in patients with type 1 diabetes
Garg, S. K., Henry, R. R., Banks, P., Buse, J. B., Davies, M. J., Fulcher, G. R., Pozzilli, P., Gesty-Palmer, D., Lapuerta, P., Simó, R., et al. (2017) · New England Journal of Medicine · doi:10.1056/nejmoa1708337 · Cited by 417
Diabetes: Advances in Diagnosis and Treatment
Nathan, D. M. (2015) · JAMA · doi:10.1001/jama.2015.9536 · Cited by 384
Metadata
- Authors
- Taylor, S. I., Blau, J. E., & Rother, K. I.
- Venue
- The Journal of Clinical Endocrinology & Metabolism
- Publisher
- The Endocrine Society
- Published
- 2015-08
- Volume
- 100
- Issue
- 8
- Pages
- 2849-2852
- ISSN
- 0021-972X (ISSN-L)
- 1945-7197
- OpenAlex
- W1834962231
- Cited by
- 560
- References
- 15
- FWCI
- 58.73
- Type
- journal article
- Language
- en
- Open access
- bronze
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