The SGLT2-inhibitor dapagliflozin improves neutropenia and neutrophil dysfunction in a mouse model of the inherited metabolic disorder GSDIb.

Authors :: Resaz R
Raggi F
Segalerba D
Lavarello C
Gamberucci A
Bosco MC
Astigiano S
Assunto A
Melis D
D'Acierno M
Veiga-da-Cunha M
Petretto A
Marcolongo P
Trepiccione F
Eva A
Source :: Molecular genetics and metabolism reports [Mol Genet Metab Rep] 2021 Oct 20; Vol. 29, pp. 100813. Date of Electronic Publication: 2021 Oct 20 (Print Publication: 2021).
Publication Year :: 2021
Abstract: Glycogen Storage Disease type 1b (GSDIb) is a genetic disorder with long term severe complications. Accumulation of the glucose analog 1,5-anhydroglucitol-6-phosphate (1,5AG6P) in neutrophils inhibits the phosphorylation of glucose in these cells, causing neutropenia and neutrophil dysfunctions. This condition leads to serious infections and inflammatory bowel disease (IBD) in GSDIb patients. We show here that dapagliflozin, an inhibitor of the renal sodium-glucose co-transporter-2 (SGLT2), improves neutrophil function in an inducible mouse model of GSDIb by reducing 1,5AG6P accumulation in myeloid cells.<br />Competing Interests: The authors declare no conflict of interest.<br /> (© 2021 Published by Elsevier Inc.)

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