Evaluation of the Modifications in the Inflammatory Response Promoted by Obesity in Monosodium Glutamate-induced Obese Rats

Aims: The purpose of this work was to investigate the inflammatory response changes caused by obesity in an experimental model of glutamate-induced obesity in rats.

Methodology: Wistar rats were injected, subcutaneously, with 4 g/kg of monosodium glutamate (MSG group) on days 2, 3, 4, 5, and 6 of life. At the age of 3 months, the male rats were tested for obesity, measuring the Lee Index, the periepididymal and retroperitoneal fat deposits, serum corticosterone, glucose, insulin tolerance, and lipid profile. The acute inflammatory response was evaluated using paw edema (induced by carrageenan or dextran), pleurisy (induced by pleural injection of carrageenan), increasing in vascular permeability (induced by intradermal injection of histamine, bradykinin, and serotonin) and leukocyte count in peripheral blood and pleural exudate. The chronic inflammatory response was evaluated by the cotton pellet-induced granuloma and air pouch methods.

Place and Duration of Study: Our study was carried out at Laboratory of Inflammation (State University of Maringá, Brazil) from January to December 2015.

Results: The MSG group presented an increase in both Lee Index and the fat deposits, glucose intolerance, high blood corticosterone levels, and insulin resistance, characterizing obesity. The paw edema was reduced in MSG group. The vascular permeability response induced by mediators of the inflammatory response (histamine, bradykinin, and serotonin) was not altered. The leukocyte migratory capacity to the pleural cavity was reduced in MSG group with the reduction of the circulating leukocyte number.

Conclusion: Our data provide evidence that acute inflammatory response is decreased in MSG animals, demonstrating the modification of the immune response caused by obesity. These changes in the innate immune response cannot be related to loss of responsiveness of tissues to inflammatory mediators. The decreasing in the blood leukocyte number associated with high levels of corticosterone were partially responsible for the suppression of acute inflammatory response.