Increase in Endogenous Glucose Production With SGLT2 Inhibition Is Unchanged by Renal Denervation and Correlates Strongly With the Increase in Urinary Glucose Excretion.
Benzhydryl Compounds
/ pharmacology
Blood Glucose
/ metabolism
Denervation
Diabetes Mellitus, Type 2
/ complications
Diabetic Nephropathies
/ drug therapy
Fasting
/ blood
Female
Glucose
/ metabolism
Glucosides
/ pharmacology
Glycosuria
/ chemically induced
Humans
Kidney
/ innervation
Kidney Transplantation
Male
Middle Aged
Sodium-Glucose Transporter 2 Inhibitors
/ pharmacology
Transplant Recipients
Journal
Diabetes care
ISSN: 1935-5548
Titre abrégé: Diabetes Care
Pays: United States
ID NLM: 7805975
Informations de publication
Date de publication:
05 2020
05 2020
Historique:
received:
30
10
2019
accepted:
25
01
2020
pubmed:
8
3
2020
medline:
27
2
2021
entrez:
8
3
2020
Statut:
ppublish
Résumé
Sodium-glucose cotransporter 2 (SGLT2) inhibition causes an increase in endogenous glucose production (EGP). However, the mechanisms are unclear. We studied the effect of SGLT2 inhibitors on EGP in subjects with type 2 diabetes (T2D) and without diabetes (non-DM) in kidney transplant recipients with renal denervation. Fourteen subjects who received a renal transplant (six with T2D [A1C 7.2 ± 0.1%] and eight non-DM [A1C 5.6 ± 0.1%) underwent measurement of EGP with [3- Following placebo in T2D, fasting plasma glucose (FPG) (143 ± 14 to 124 ± 10 mg/dL; Renal denervation in patients who received a kidney transplant failed to block the DAPA-mediated stimulation of EGP in both individuals with T2D and non-DM subjects. The DAPA-stimulated rise in EGP is strongly related to the increase in UGE, blunting the decline in FPG.
Identifiants
pubmed: 32144165
pii: dc19-2177
doi: 10.2337/dc19-2177
pmc: PMC7171949
doi:
Substances chimiques
Benzhydryl Compounds
0
Blood Glucose
0
Glucosides
0
Sodium-Glucose Transporter 2 Inhibitors
0
dapagliflozin
1ULL0QJ8UC
Glucose
IY9XDZ35W2
Banques de données
ClinicalTrials.gov
['NCT03168295']
Types de publication
Journal Article
Randomized Controlled Trial
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
1065-1069Subventions
Organisme : NIDDK NIH HHS
ID : R01 DK107680
Pays : United States
Informations de copyright
© 2020 by the American Diabetes Association.
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