Somatostatin: a possible mediator of the long-term effects of experimental vertical gastrectomy on glucose metabolism in rats?

• Published in: Journal of gastrointestinal surgery 2024-06, Vol.28 (6), p.923-932
• Main Authors: Pérez-Arana, Gonzalo-Martín, González-Domínguez, Álvaro, Visiedo, Francisco, Gómez, Alfredo Díaz, Bancalero-de los Reyes, José, Camacho-Ramírez, Alonso, Ribelles-García, Antonio, Almorza-Gomar, David, Gracia-Romero, Manuel, Casar-García, Juan, Prada-Oliveira, José-Arturo
• Format: Article
• Language: English
• Subjects: Animals; Blood Glucose - metabolism; Duodenum - metabolism; Duodenum - surgery; Gastrectomy - methods; Insulin - blood; Insulin-Secreting Cells - drug effects; Insulin-Secreting Cells - metabolism; Male; Pancreas; Rats; Rats, Wistar; Receptors, Somatostatin - metabolism; Sleeve gastrectomy; Somatostatin; Somatostatin - analogs & derivatives
• ISSN: 1091-255X; 1873-4626; 1873-4626
• DOI: 10.1016/j.gassur.2024.03.035

Sleeve gastrectomy (SG) is one of the most commonly performed bariatric surgeries. SG treats type 2 diabetes mellitus better than several drugs. The mechanisms that underlie this phenomenon are not clear. This study proposed that somatostatin (SST) isoforms SST-14 and SST-28 are key in the carbohydrate after SG. Surgeries were performed on 3 groups of Wistar rats: the fasting, surgery control, and SG groups. Plasma levels of glucose, insulin, SST-14, and SST-28 were measured at 2 survival periods after surgery. Islet SST receptor (SSTR) and cell populations were studied. We performed a pasireotide (SST-28 analogue) infusion assay in another group of rats to confirm the influence of SST-28 plasma levels on the delta-cell population. This study found an elevation in the insulin response after SG in animals but a decrease in the insulin response over the long term with a loss of beta-cell mass. An increase in duodenal SST-28–producing cells in the duodenum and a loss of pancreatic SST-14–producing cells were observed after SG in animals but not in controls. The expression of SSTR type 5 in delta-cell populations from each group and the ability of the pasireotide infusion assay to decrease the delta-cell population indicated the effect of SST-28 plasma levels on delta-cell maintenance. After SG initiates a compensatory response in the duodenum, beta-cell mass is depleted after loss of the brake that regulates SST-14 at the paracrine level in a nonobese, normoglycemic rat model. This was an experimental model, with no clinical translation to the human clinic, with a preliminary importance regarding new pathophysiologic perspectives or pathways.