Relationship between obesity and intestinal lamina propria cells function in insulin resistance development

• Grant number: 15/18121-4
• Support Opportunities: Scholarships in Brazil - Post-Doctorate
• Effective date (Start): October 01, 2015
• Effective date (End): June 30, 2017
• Field of knowledge: Biological Sciences - Immunology - Cellular Immunology
• Principal Investigator: Niels Olsen Saraiva Câmara
• Grantee: Angela Castoldi
• Host Institution: Instituto de Ciências Biomédicas (ICB). Universidade de São Paulo (USP). São Paulo , SP, Brazil
• Associated research grant: 12/02270-2 - New cellular, molecular and immunological mechanisms involved in acute and chronic renal injury: the search for new therapeutical approaches, AP.TEM

Abstract

Insulin resistance due to obesity is linked to inflammation in several tissues. Although to be a lymphoid tissue, the intestine recognizes and secretes a variety of molecules, but the role of intestinal lamina propria cells in the development of obesity and whether the activation of these cells regulates the development of insulin resistance is still unknown. It is known that during obesity, microbial changes induce increased fermentation and production of short chain fatty acids, which contributes to increased energy uptake and lipid absorption from the intestine, increased intestinal permeability and intestinal inflammation which is correlated to insulin resistance development. The importance of studying and understanding the associated factors in the development of obesity is explained by the correlation between obesity and insulin resistance to the development of several diseases and, among them, the progression of kidney disease. Studies showed that there is an association between secretion of inflammatory molecules during obesity/insulin resistance, development of glomerulosclerosis and others kidney diseases. In addition, changes in the metabolism of immune system cells during obesity can be directly correlated with changes in renal function. Also, microbial fermentation products have been shown in the development of kidney injury and this process may be dependent on the gut immune system activation during obesity.

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)

CASTOLDI, ANGELA; ANDRADE-OLIVEIRA, VINICIUS; AGUIAR, CRISTHIANE FAVERO; AMANO, MARIANE TAMI; LEE, JENNIFER; MIYAGI, MARCELLI TERUMI; LATANCIA, MARCELA TEATIN; BRAGA, TARCIO TEODORO; DA SILVA, MARINA BURGOS; IGNACIO, ALINE; et al. Dectin-1 Activation Exacerbates Obesity and Insulin Resistance in the Absence of MyD88. CELL REPORTS, v. 19, n. 11, p. 2272-2288, JUN 13 2017. (15/18121-4, 11/15682-4, 12/02270-2)

CASTOLDI, ANGELA; DE SOUZA, CRISTIANE NAFFAH; SARAIVA CAMARA, NIELS OLSEN; MORAES-VIEIRA, PEDRO M.. The Macrophage Switch in Obesity Development. FRONTIERS IN IMMUNOLOGY, v. 6, JAN 5 2016. (15/18121-4, 11/15682-4, 12/02270-2, 14/10910-7)

FERREIRA FELIZARDO, RAPHAEL JOSE; CASTOLDI, ANGELA; ANDRADE-OLIVEIRA, VINICIUS; SARAIVA CAMARA, NIELS OLSEN. The microbiota and chronic kidney diseases: a double-edged sword. CLINICAL & TRANSLATIONAL IMMUNOLOGY, v. 5, JUN 2016. (12/15205-4, 15/18121-4)