RT journal article
T1 Somatostatin: From a supporting actor to the protagonist to explain the long-term effect of sleeve gastrectomy on glucose metabolism.
A1 Pérez Arana, Gonzalo Martín
A1 Díaz Gómez, Alfredo Luis
A1 Bancalero-de los Reyes, José
A1 Camacho Ramírez, Alonso
A1 Ribelles García, Antonio
A1 Almorza Gomar, David
A1 Gracia Romero, Manuel Ángel
A1 Mateo-Gavira, Isabel
A1 Prada Oliveira, José Arturo
A2 Anatomía y Embriología Humana
A2 Estadística e Investigación Operativa
K1 Pancreas
K1 Sleeve gastrectomy
K1 Type 2 diabetes mellitus
K1 Bariatric surgeries
K1 Somatostatin
AB BACKGROUND: Bariatric/metabolic surgery has become the most effective treatment against type 2 Diabetes mellitus (T2DM). The role of many gastrointestinal hormones in T2DM has been proposed, but the pathophysiological models described vary greatly depending on the anatomical rearrangements after surgery. We focus on somatostatin as a common factor in two of the most commonly performed surgical procedures in a healthy rodent model. We performed sleeve gastrectomy (SG) and Roux-en-Y gastric bypass (RYGB) and also an experimental surgery without gastric involvement (intestinal resection of 50 % jejunum-ileum portion -IR50 %).METHODS: We used five groups of Wistar rats: fasting control, sham-operated, SG-operated, RYGB-operated and IR50-operated. We analysed several parameters 4 and 23 weeks after surgery: plasma SST-14/28 fractions, plasma glucose, insulin release and SST-producing cell expression in the duodenum and pancreatic islets.RESULTS: Numerous SST-producing cells in the duodenum but a low number in the pancreas and a long-term loss of glucose tolerance were observed in SG and RYGB animals. Additionally, a high plasma SST-28 fraction was found in animals after SG but not after RYGB. Finally, IR50 animals showed no differences versus controls.CONCLUSIONS: In our SG model the amplitude of insulin response after metabolic surgeries, is mediated by SST-28 plasma levels derived from the proportional compensatory effect of gastric SST-producing tissue ablation. In addition, a strong compensatory response to the surgical loss of gastric SST-producing cells, leads to long-term loss of insulin production after SG but not in the others.Copyright © 2022 The Author(s). Published by Elsevier GmbH.. All rights reserved.
PB ELSEVIER
SN 1618-0402
YR 2022
FD 2022-12
LK http://hdl.handle.net/10498/27881
UL http://hdl.handle.net/10498/27881
LA eng
DS Repositorio Institucional de la Universidad de Cádiz
RD 11-nov-2026