Open AccessAir pollution participates in genesis of obesity through the activation of hypothalamic
Author(s) -
Clara Machado Campolim,
Patrícia de Oliveira Prada,
Clílton Kraüss de Oliveira Ferreira,
Vitor Ferreira Boico,
Olívia Pizetta Zordão,
Soraia K.P. Costa,
Mariana Matera Veras,
Paulo Hilário Nascimento Saldiva
Publication year - 2018
Publication title -
revista dos trabalhos de iniciação científica da unicamp
Language(s) - English
Resource type - Journals
ISSN - 2596-1969
DOI - 10.20396/revpibic262018311
Subject(s) - leptin , tlr4 , inflammation , hypothalamus , endocrinology , medicine , energy homeostasis , leptin receptor , immune system , biology , obesity , hormone , immunology
Air pollution is involved in several processes harmful to health. PM2,5 is the most associated with the induction of chronic inflammation. Hypothalamus regulates the energy homeostasis thought metabolic, neural and hormonal signals. Leptin signaling participates in this process, and hypothalamic inflammation may induce leptin resistance. TLR4 is an innate immune receptor capable of triggering subclinical inflammation, and one of its agonists is LPS, which is known be present in the PM2.5 composition. Polluted C57 mice had increased adiposity due to hyperphagia and lower energy expenditure, caused by leptin resistance. The TLR4 gene expression was elevated in the hypothalamus of polluted C57. The TLR4 deletion protected the animal from obesity, glucose intolerance, and leptin resistance when exposed to PM2.5. Together, these results suggest that air pollution induces hypothalamic leptin resistance by the activation of inflammatory pathways, probably involving TLR4.