Title: Reduced Glucose-Induced Insulin Secretion in Low-protein-fed Rats Is Associated With Altered Pancreatic Islets Redox Status
Author: Cappelli Ap; Zoppi Cc; Silveira, Leonardo R.; Barbosa-sampaio, H.C.; Boschero, A. C; Carneiro, Everardo M.
Is part of: Journal of Cellular Physiology (Print)p. 1 -
Citation: Cappelli Ap; Zoppi Cc; Silveira, Leonardo R.; Barbosa-sampaio, H.C.; Boschero, A. C; Carneiro, Everardo M.; Reduced Glucose-Induced Insulin Secretion in Low-protein-fed Rats Is Associated With Altered Pancreatic Islets Redox Status. Journal of Cellular Physiology (Print), v., p. 1-, 2017
Abstract: In the present study, we investigated the relationship between early life protein malnutrition-induced redox imbalance, and reduced glucose-stimulated insulin secretion. After weaning, male Wistar rats were submitted to a normal-protein-diet (17%-protein, NP) or to a low-protein-diet (6%-protein, LP) for 60 days. Pancreatic islets were isolated and hydrogen peroxide (H2O2), oxidized (GSSG) and reduced (GSH) glutathione content, CuZn-superoxide dismutase (SOD1), glutathione peroxidase (GPx1) and catalase (CAT) gene expression, as well as enzymatic antioxidant activities were quantified. Islets that were pre-incubated with H2O2 and/or N-acetylcysteine, were subsequently incubated with glucose for insulin secretion measurement. Protein malnutrition increased CAT mRNA content by 100%. LP group SOD1 and CAT activities were 50% increased and reduced, respectively. H2O2 production was more than 50% increased whereas GSH/GSSG ratio was near 60% lower in LP group. Insulin secretion was, in most conditions, approximately 50% lower in LP rat islets. When islets were pre-incubated with H2O2 (100M), and incubated with glucose (33mM), LP rats showed significant decrease of insulin secretion. This effect was attenuated when LP islets were exposed to N-acetylcysteine.
Funding: Fundacao de Amparo a Pesquisa do Estado de Sao Paulo, Grant numbers: 06/58822-2, 07/50365-4; Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq); Instituto Nacional de C&T: Obesidade e Diabetes