STUDY OF METABOLIC MODULATION OF MICROGLIA BY LEPTIN

Publicado em 09/06/2023 - ISBN: 978-85-5722-785-9

Título do Trabalho
STUDY OF METABOLIC MODULATION OF MICROGLIA BY LEPTIN
Autores
  • Wilias Greison Silva Santos
  • Gisele de Castro
  • Monara Kaelle Angelim
  • JULIANA EDELVACY LIMA PINTO
  • GUILHERME RIBEIRO
  • Ana Julia Estumano Martins
  • JEFFERSON ANTONIO DE CASTRO DOS SANTOS
  • Webster Leonardo Guimarães da Costa
  • Lincon Felipe Lima Silva
  • JOÃO VICTOR VIRGILIO DA SILVA
  • Larissa Menezes dos Reis
  • Pedro Manoel Mendes de Moraes Vieira
Modalidade
Apresentação de Pôster
Área temática
Imunologia
Data de Publicação
09/06/2023
País da Publicação
Brasil
Idioma da Publicação
Inglês
Página do Trabalho
https://www.even3.com.br/anais/v-gbmeeting/609420-study-of-metabolic-modulation-of-microglia-by-leptin
ISBN
978-85-5722-785-9
Palavras-Chave
ObR, Obesity, Leptin
Resumo
Obesity occurs, most of the time, when food intake exceeds energy expenditure, causing excessive accumulation of fat or white adipose tissue in the body. In obese people, the long-chain fatty acid palmitate is increased and directly accumulates in the hypothalamus, leading to metabolic disturbances, inflammation, neurodegeneration, and insulin resistance. Obesity is linked to the process of resistance to leptin, a hormone derived from adipose tissue, which plays a central role in regulating energy balance, suppressing food intake, and promoting energy expenditure. In the central nervous system (CNS), increased levels of leptin and palmitate are detected by resident microglia and macrophages, leading to enlargement of the hypothalamus. However, the extent to which leptin influences microglial activation during obesity remains uncertain. In this context, this work aimed to study microglia in the face of obesity and hyperleptinemia. To understand how palmitate modulates microglia, we treated in vitro microglia from CX3CR1CreER/+:R26DsRed/+ animals up to three days old (P0-P3) with palmitate (400µM). Palmitate seems to increase the expression of TNF-? and IL-6, without affecting its sense, not being able to modulate the mitochondrial muscle and the glycolytic rate. However, palmitate treatment directly modulated mitochondrial morphology, taking into account its ramifications. Next, we sought to understand the mechanisms by which leptin modulates microglia. Microglia were pre-treated with leptin (100ng/ml) and activated with palmitate (400µM) for 6 hours. We observed that leptin acted as a negative regulator in the presence of palmitate, inhibiting the expression and secretion of IL-6 and TNF. Combined leptin+palmitate treatment increased mitochondrial respiration and glycolytic rate compared to untreated microglia. Then, the microglia of the CX3CR1CreER/+:R26DsRed/+Obrfl/fl animals were treated with tamoxifen (2.5 µM). This treatment allows the expression of Cre recombinase to promote the deletion of the leptin receptor (Obr). Our data show that the microglial inflammatory profile is ObR-dependent since microglia isolated from palmitate-activated ObR-deficient animals did not alter the expression of inflammatory cytokines. Thus, our partials are that leptin acts as a negative regulator on microglia in the presence of palmitate.
Título do Evento
V GBMeeting
Cidade do Evento
Campinas
Título dos Anais do Evento
Anais do GBMeeting: Encontro Anual da Pós Graduação em Genética e Biologia Molecular da UNICAMP
Nome da Editora
Even3
Meio de Divulgação
Meio Digital
DOI
LinkObter o DOI

Como citar

SANTOS, Wilias Greison Silva et al.. STUDY OF METABOLIC MODULATION OF MICROGLIA BY LEPTIN.. In: Anais do GBMeeting: Encontro Anual da Pós Graduação em Genética e Biologia Molecular da UNICAMP. Anais...Campinas(SP) Unicamp, 2023. Disponível em: https//www.even3.com.br/anais/v-gbmeeting/609420-STUDY-OF-METABOLIC-MODULATION-OF-MICROGLIA-BY-LEPTIN. Acesso em: 19/06/2024

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