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Obesity-induced inflammation, alterations in the microbiota and their effects on the enteric nervous system: study in an experimental model of zebrafish

Grant number: 15/21644-9
Support type:Scholarships in Brazil - Doctorate
Effective date (Start): February 01, 2016
Effective date (End): October 31, 2020
Field of knowledge:Biological Sciences - Immunology
Principal Investigator:Niels Olsen Saraiva Câmara
Grantee:Camila Ideli Morales Fenero
Home 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
Associated scholarship(s):18/05658-8 - Mechanism of action of a bacterial anti-inflammatory protein, AimA, BE.EP.DR

Abstract

Diets with high levels of carbohydrates and fats, physical inactivity and stress are inducers of metabolic disorders such as insulin resistance, changes in microbiota and obesity. In the last decade, evidence has linked obesity with a state of chronic low-level inflammation, characterized by a release of cytokines by adipose tissue with a predominantly mononuclear inflammatory infiltrate. The microbiota has also been linked to obesity and metabolic changes, influencing weight gain, insulin sensitivity and the inflammatory state, both in the intestine and other organs. Intestinal functions as motility, secretion of hormones, blood flow modulation and nutrient uptake are controlled by the enteric nervous system (ENS) and are altered in obesity. However, the morphological and physiological changes in glial cells and enteric neurons as a result of inflammation, are largely unexplored points. Even less is known about the influence of microbiota in these events. The zebrafish is being target in the study of human pathologies and emerges as an excellent model for the in vivo analysis of the nervous system and the intestine due to features such as transparency, large numbers of animals per crossing, rapid development and low maintenance costs. Thus, we hypothesized that changes in the microbiota, induced by the inflammation resulting from obesity are responsible for changes in ENS. Thus, the objective of this work is to study the ENS changes during obesity, correlating them with the inflammatory state and the commensal microbiota, using a model of obesity induced by diet in juvenile fish. We hope to demonstrate that obesity model in juvenile fish is a great experimental alternative, and can give results on disease mechanisms, such as obesity.