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SAA participation in the genesis of diabetes

Grant number: 18/17986-0
Support Opportunities:Scholarships in Brazil - Scientific Initiation
Start date: January 01, 2019
End date: December 31, 2020
Field of knowledge:Biological Sciences - Pharmacology - Biochemical and Molecular Pharmacology
Principal Investigator:Elaine Hatanaka Dermargos
Grantee:Aline Correia Costa de Morais
Host Institution: Centro de Ciências Biológicas e da Saúde. Universidade Cruzeiro do Sul (UNICSUL). São Paulo , SP, Brazil

Abstract

Decreased insulin secretion by pancreatic ² cells may be mediated by chronic inflammation, lipotoxicity, or amyloidosis. Serum amyloid A (SAA), a classical acute phase protein, induces the production of cytokines in leukocytes. Persistently high SAA levels characterize a number of metabolic disorders, such as obesity. The biological effects of this protein are far from being fully understood although the role of SAA is in most forms of inflammation, infection and tissue damage. We hypothesized that chronic pancreatic exposure to SAA may lead to changes in the production of inflammatory/oxidative mechanisms, participating in the genesis of type 2 diabetes. For this, we will investigate the effects of SAA on pancreatic ²-cell function.

News published in Agência FAPESP Newsletter about the scholarship:
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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)
HATANAKA, E.; BRAGA BARROS SILVA, M.; CORREIA COSTA DE MORAIS, A.; MASAHIRO MURATA, G.; DERMARGOS, A.. Serum amyloid A induces cytokine and growth factor production in pancreatic beta cells. FEBS OPEN BIO, v. 9, p. 1-pg., . (18/17986-0)