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Molecular mechanisms involved in the dysfunction and death of pancreatic beta cells in Diabetes Mellitus: strategies for the prevention of islet dysfunction and for islet mass recuperation in different cellular and animal models

Abstract

Diabetes Mellitus (DM1 or DM2) is defined as a syndrome of chronic hyperglycemia due to the lack of insulin production that results from the reduction of beta cell mass which, in turn, originated from an increase in cell apoptosis and/or deficient beta cell regeneration. In DM2, reduction of beta cell mass is frequently accompanied by an increase in insulin resistance in muscle, adipose, and hepatic tissues. Despite the enormous amount of information present in the literature concerning the diabetic syndrome, the molecular mechanisms underlying this syndrome is not completely known. Following our preceding studies, in the present Project we will study the mechanisms responsible for the loss of the mass and functionality of pancreatic islets in different animal models (protein malnutrition, obesity, dislipidemia, and induced DM2) and cell types. We will also study the mechanisms involved in the increase in islet cell mass in different periods of life (fetal, neonatal and pregnancy). In the former, the focus will be on the participation of ER stress, alteration in Ca2+ handling, and increase in the oxidative stress. In the later, the attention will centered on the signaling pathways that control the increase in mass and functionality of the pancreatic islets as well as on possible benefits to the islets by amino acids supplementation or by the use of peptides that showed previously to be able to restore islet cell viability. (AU)

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Scientific publications
(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)
FERREIRA, SANDRA M.; COSTA-JUNIOR, JOSE M.; KURAUTI, MIRIAN A.; LEITE, NAYARA C.; ORTIS, FERNANDA; REZENDE, LUIZ F.; BARBOSA, HELENA C.; BOSCHERO, ANTONIO C.; SANTOS, GUSTAVO J.. ARHGAP21 Acts as an Inhibitor of the Glucose-Stimulated Insulin Secretion Process. FRONTIERS IN ENDOCRINOLOGY, v. 11, . (11/12050-7, 11/09012-6)
LEITE, NAYARA CARVALHO; DE PAULA, FLAVIA; BORCK, PATRICIA CRISTINE; VETTORAZZI, JEAN FRANCIESCO; SOUTO BRANCO, RENATO CHAVES; LUBACZEUSKI, CAMILA; BOSCHERO, ANTONIO CARLOS; ZOPPI, CLAUDIO CESAR; CARNEIRO, EVERARDO MAGALHAES. Protein malnutrition potentiates the amplifying pathway of insulin secretion in adult obese mice. SCIENTIFIC REPORTS, v. 6, . (13/07607-8, 11/19536-2, 11/09012-6)

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