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dc.contributorVall d'Hebron Barcelona Hospital Campus
dc.contributor.authorCuidin Mihai, Andreea
dc.contributor.authorSánchez, Marta
dc.contributor.authorHernández Hernández, Irene
dc.contributor.authorCordero Vázquez, Efráin Santiago
dc.contributor.authorFidilio Meli, Enzamaría
dc.contributor.authorComas Martínez, Marta
dc.contributor.authorGonzalez Junyent, Carla
dc.contributor.authorLopez Martin, Natividad
dc.contributor.authorVilallonga Puy, Ramón
dc.contributor.authorGiralt Arnaiz, Marina
dc.contributor.authorFerrer Costa, Roser
dc.contributor.authorHernández Pascual, Cristina
dc.contributor.authorSimó Canonge, Rafael
dc.date.accessioned2021-12-27T13:23:42Z
dc.date.available2021-12-27T13:23:42Z
dc.date.issued2021-06
dc.identifier.citationCiudin A, Sánchez M, Hernandez I, Cordero E, Fidilio E, Comas M, et al. Canagliflozin: A New Therapeutic Option in Patients That Present Postprandial Hyperinsulinemic Hypoglycemia after Roux-en-Y Gastric Bypass: A Pilot Study. Obes Facts. 2021 Jun;14:291–297.
dc.identifier.issn1662-4025
dc.identifier.urihttp://hdl.handle.net/11351/6737
dc.descriptionBariatric surgery; Pharmacological therapy; Postprandial hypoglycemia
dc.description.abstractIntroduction: Roux-en-Y gastric bypass (RYGB) is the most common surgical procedure for morbid obesity. However, it can present serious late complications, like postprandial hyperinsulinemic hypoglycemia (PHH). Recent data suggested an increase in intestinal SGLT-1 after RYGB. However, there is no data on the inhibition of SGLT-1 to prevent PHH in patients with prior RYBG. On this basis, we aimed to evaluate (a) the effect of canagliflozin 300 mg on the response to 100 g glucose overload (oral glucose tolerance test [OGTT]); (b) the pancreatic response after intra-arterial calcium stimulation in the context of PHH after RYGB. Materials and Methods: This is a prospective pilot study including patients (n = 21) with PHH after RYGB, matched by age and gender with healthy controls (n = 5). Basal OGTT and after 2 weeks of daily 300 mg of canagliflozin was performed in all cases. In addition, venous sampling after intra-arterial calcium stimulation of the pancreas was performed in 10 cases. Results: OGTT after canagliflozin showed a significant reduction of plasma glucose levels (minute 30: 161.5 ± 36.22 vs. 215.9 ± 58.11 mg/dL; minute 60: 187.46 ± 65.88 vs. 225.9 ± 85.60 mg/dL, p < 0.01) and insulinemia (minute 30: 95.6 ± 27.31 vs. 216.35 ± 94.86 mg/dL, p = 0.03; minute 60: 120.85 ± 94.86 vs. 342.64 ± 113.32 mIU/L, p < 0.001). At minute 180, a significant reduction (85.7%) of the rate of hypoglycemia was observed after treatment with canagliflozin (p < 0.00001). All cases presented normal pancreatic response after intra-arterial calcium administration. Conclusion: Canagliflozin (300 mg) significantly decreased glucose absorption and prevented PHH after 100 g OGTT in patients with RYGB. Our results suggest that canagliflozin could be a new therapeutic option for patients that present PHH after RYGB.
dc.language.isoeng
dc.publisherKarger
dc.relation.ispartofseriesObesity Facts;14
dc.rightsAttribution-NonCommercial 4.0 International
dc.rights.urihttp://creativecommons.org/licenses/by-nc/4.0/
dc.sourceScientia
dc.subjectHipoglucèmia - Tractament
dc.subjectObesitat - Cirurgia - Complicacions
dc.subject.meshHypoglycemia
dc.subject.mesh/drug therapy
dc.subject.meshGastric Bypass
dc.subject.mesh/adverse effects
dc.titleCanagliflozin: A New Therapeutic Option in Patients That Present Postprandial Hyperinsulinemic Hypoglycemia after Roux-en-Y Gastric Bypass: A Pilot Study
dc.typeinfo:eu-repo/semantics/article
dc.identifier.doi10.1159/000515598
dc.subject.decshipoglucemia
dc.subject.decs/farmacoterapia
dc.subject.decsderivación gástrica
dc.subject.decs/efectos adversos
dc.relation.publishversionhttps://doi.org/10.1159/000515598
dc.type.versioninfo:eu-repo/semantics/publishedVersion
dc.audienceProfessionals
dc.contributor.organismesInstitut Català de la Salut
dc.contributor.authoraffiliation[Ciudin A, Hernández C, Simó R] Vall d’Hebron Institut de Recerca (VHIR), Barcelona, Spain. Universitat Autònoma de Barcelona, Bellaterra, Spain. CIBER de Diabetes y Enfermedades Metabólicas Asociadas, Instituto de Salud Carlos III, Barcelona, Spain. Servei d’Endocrinologia i Nutrició, Vall d’Hebron Hospital Universitari, Barcelona, Spain. [Sánchez M] Endocrinology and Nutrition Department, Hospital Universitario Gran Canaria Doctor Negrín, Las Palmas, Spain. [Hernandez I, Cordero E, Comas M, Lopez N] Servei d’Endocrinologia i Nutrició, Vall d’Hebron Hospital Universitari, Barcelona, Spain. [Fidilio E] Vall d’Hebron Institut de Recerca (VHIR), Barcelona, Spain. Universitat Autònoma de Barcelona, Bellaterra, Spain. [Gonzalez C] Servei d’Angioradiologia, Vall d’Hebron Hospital Universitari, Barcelona, Spain. [Vilallonga R] Unitat de Cirurgia Endocrina, Metabòlica i Bariàtrica, Vall d’Hebron Hospital Universitari, Barcelona, Spain. [Giralt M] Servei de Bioquímica Clínica, Vall d’Hebron Hospital Universitari, Barcelona, Spain. [Ferrer R] Vall d’Hebron Institut de Recerca (VHIR), Barcelona, Spain. Universitat Autònoma de Barcelona, Bellaterra, Spain. Servei de Bioquímica Clínica, Vall d’Hebron Hospital Universitari, Barcelona, Spain
dc.identifier.pmid33965935
dc.identifier.wos000652267700001
dc.rights.accessrightsinfo:eu-repo/semantics/openAccess


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