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Evaluation of NOD2 receptor role in insulin resistance and type 2 diabetes

Grant number: 14/15462-2
Support Opportunities:Scholarships in Brazil - Scientific Initiation
Effective date (Start): August 01, 2014
Effective date (End): February 29, 2016
Field of knowledge:Biological Sciences - Immunology - Cellular Immunology
Principal Investigator:Daniela Carlos Sartori
Grantee:Larissa Marfori Sampaio Martins
Host Institution: Faculdade de Medicina de Ribeirão Preto (FMRP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil
Associated research grant:12/10395-0 - Role of NLRs receptors in immunoregulation mechanisms of the type 1 and 2 diabetes: identification of potential therapeutic targets, AP.JP


The etiology of type 2 diabetes (T2DM) is related to genetic, environmental and dietary factors. Recent studies have demonstrated the importance of NOD2 signaling pathway in the maintenance of homeostasis of the immune system and the gut microbiota. Unlike the human genome, the genome of microorganisms present in the gut microbiota is able to dynamic changes in the configuration of its components in order to adaptation of an individual component or a community in response to the type of food, some abnormality or antibioti use. The causal interaction between gut microbiota and obesity has been reported in mice germ-free colonized with gut microbiota of obese ob/ob mice that showed greater weight gain compared to those who received the microbiota of non-obese animals. This study infers that the microbiota is involved in the control of energy metabolism. Another mechanism by which the microbiome contributes metabolic disorders would be initiating a systemic inflammation. Thus, we aim to evaluate the importance of theNOD2 receptor in the insulin resistance and T2D development, such as to test the interference of microbiota intestinal in this process.

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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)
MARTINS, LARISSA M. S.; PEREZ, MALENA M.; PEREIRA, CAMILA A.; COSTA, FREDERICO R. C.; DIAS, MURILO S.; TOSTES, RITA C.; RAMOS, SIMONE G.; DE ZOETE, MARCEL R.; RYFFEL, BERNHARD; SILVA, JOAO S.; et al. Interleukin-23 promotes intestinal T helper type17 immunity and ameliorates obesity-associated metabolic syndrome in a murine high-fat diet model. IMMUNOLOGY, v. 154, n. 4, p. 624-636, . (14/15462-2)

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