J Gastrointest Surg. 2024 Apr 2:S1091-255X(24)00398-6. doi: 10.1016/j.gassur.2024.03.035. Online ahead of print.
ABSTRACT
OBJECTIVE: Sleeve gastrectomy (SG) is one of the most commonly performed bariatric surgeries. SG treats diabetes (T2D) better than many drugs. The mechanisms that underlie this phenomenon are not clear. We propose that somatostatin (SST) isoforms SST-14 and SST-28 are key in the carbohydrate after SG.
METHODS: We performed surgeries on three groups of Wistar rats: the fasting (FC), surgery control (Sham), and SG groups. We measured plasma levels of glucose, insulin, SST-14 and SS-28 at two survival periods after surgery. Islet somatostatin receptor (SSTR) and cell populations were studied. We performed a pasireotide (SST-28 analog) infusion assay in another group of rats to confirm the influence of SST-28 plasma levels on the delta-cell population.
RESULTS: We found an elevation in the insulin response after surgery in SG 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 found after SG but not in controls. The expression of SSTR-5 in delta-cell populations from each group and the ability of the pasireotide infusion assay to decrease the delta-cell population indicate the effect of SST-28 plasma levels on delta-cell maintenance.
CONCLUSION: 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 non-obese, normoglycemic model of rat. This is an experimental model, with no-clinical translation to human clinic, with a preliminary importance about new pathophysiological perspectives or pathways.
PMID:38574966 | DOI:10.1016/j.gassur.2024.03.035
