Acute inflammation in the genesis of obesity: experimental model focused on the protein serum amyloid a (SAA) as an adipose tissue marker of inflammation and hypertrophy

• Grant number: 11/24052-4
• Support Opportunities: Regular Research Grants
• Start date: April 01, 2012
• End date: March 31, 2014
• Field of knowledge: Biological Sciences - Physiology - General Physiology
• Principal Investigator: Ana Campa
• Grantee: Ana Campa
• Host Institution: Faculdade de Ciências Farmacêuticas (FCF). Universidade de São Paulo (USP). São Paulo , SP, Brazil

Abstract

The inflammation resulting from obesity is well characterized. More recently it has been discussed, if obesity could be a consequence of the inflammatory process. It is known that lipopolysaccharide (LPS), administered in very low doses by continuous infusion (mimicking the condition of endotoxemia caused by intestinal microbiota), induces insulin resistance, obesity and diabetes in mice. In this study we attempted to assess if acute inflammation is capable of inducing obesity. This hypothesis will be tested by serial induction of acute inflammation, caused by intra-peritoneal administration of high doses of LPS in swiss webster mice. Analysis will be made in the serum, carcass, adipose tissue and isolated adipocytes. One of the striking systemic events that occurs during an acute phase is the synthesis of the protein serum amyloid A (SAA). Our interest in SAA is derived from results obtained in our laboratory that show an action on proliferation, differentiation and lipolysis of pre-adipocytes 3T3-L1. Therefore, our interest is to assess the relationship between the generated mediators in acute inflammation and the genesis of obesity, through the effect of serum from inflamed animals on the proliferation, differentiation and lipolysis of pre-adipocytes 3T3-L1. As a consequence for the effects of SAA that we describe on adipogenesis, will be evaluated the contribution of SAA as a link between inflammation and obesity, through the overexpression of SAA in 3T3-L1 cells. (AU)

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)

DE OLIVEIRA, EDSON M.; ASCAR, THAIS P.; SILVA, JACQUELINE C.; SANDRI, SILVANA; MIGLIORINI, SILENE; FOCK, RICARDO A.; CAMPA, ANA. Serum amyloid A links endotoxaemia to weight gain and insulin resistance in mice. Diabetologia, v. 59, n. 8, p. 1760-1768, AUG 2016. (10/18498-7, 11/24052-4)

DE OLIVEIRA, EDSON M.; VISNIAUSKAS, BRUNA; TUFIK, SERGIO; ANDERSEN, MONICA L.; CHAGAS, JAIR R.; CAMPA, ANA. Serum Amyloid A Production Is Triggered by Sleep Deprivation in Mice and Humans: Is That the Link between Sleep Loss and Associated Comorbidities?. NUTRIENTS, v. 9, n. 3, MAR 2017. (10/18498-7, 11/24052-4)

DE OLIVEIRA, EDSON MENDES; SILVA, JACQUELINE C.; ASCAR, THAIS P.; SANDRI, SILVANA; MARCHI, ALEXANDRE F.; MIGLIORINI, SILENE; NAKAYA, HELDER T., I; FOCK, RICARDO A.; CAMPA, ANA. Acute Inflammation Is a Predisposing Factor for Weight Gain and Insulin Resistance. PHARMACEUTICS, v. 14, n. 3, p. 13-pg., 2022-03-01. (11/24052-4, 10/18498-7)