Search

Your search keyword '"Dias, Sandra Martha Gomes"' showing total 2 results
Start Over Author "Dias, Sandra Martha Gomes" Publisher american diabetes association
2 results on '"Dias, Sandra Martha Gomes"'

1. Leptin Signaling Suppression in Macrophages Improves Immunometabolic Outcomes in Obesity

Author

Monteiro, Lauar de Brito, primary, Prodonoff, Juliana Silveira, primary, Aguiar, Cristhiane Favero de, primary, Correa-da-Silva, Felipe, primary, Castoldi, Angela, primary, Bakker, Nikki van Teijlingen, primary, Davanzo, Gustavo Gastão, primary, Castelucci, Bianca, primary, Pereira, Jéssica Aparecida da Silva, primary, Curtis, Jonathan, primary, Büscher, Jörg, primary, Reis, Larissa Menezes dos, primary, Castro, Gisele, primary, Ribeiro, Guilherme, primary, Virgílio-da-Silva, João Victor, primary, Adamoski, Douglas, primary, Dias, Sandra Martha Gomes, primary, Consonni, Silvio Roberto, primary, Jr, Jose Donato, primary, Pearce, Edward J., primary, Câmara, Niels Olsen Saraiva, primary, and Manoel Moraes-Vieira, Pedro, primary

Published
2022
Full Text
View/download PDF

2. Leptin Signaling Suppression in Macrophages Improves Immunometabolic Outcomes in Obesity.

Author

Monteiro, Lauar de Brito, Prodonoff, Juliana Silveira, Favero de Aguiar, Cristhiane, Correa-da-Silva, Felipe, Castoldi, Angela, Bakker, Nikki van Teijlingen, Davanzo, Gustavo Gastão, Castelucci, Bianca, Pereira, Jéssica Aparecida da Silva, Curtis, Jonathan, Büscher, Jörg, Reis, Larissa Menezes dos, Castro, Gisele, Ribeiro, Guilherme, Virgílio-da-Silva, João Victor, Adamoski, Douglas, Dias, Sandra Martha Gomes, Consonni, Silvio Roberto, Donato Jr., Jose, and Pearce, Edward J.

Subjects
OBESITY, LEPTIN, ANIMAL experimentation, INFLAMMATION, MACROPHAGES, INSULIN resistance, MICE, ADIPOSE tissues
Abstract

Obesity is a major concern for global health care systems. Systemic low-grade inflammation in obesity is a major risk factor for insulin resistance. Leptin is an adipokine secreted by the adipose tissue that functions by controlling food intake, leading to satiety. Leptin levels are increased in obesity. Here, we show that leptin enhances the effects of LPS in macrophages, intensifying the production of cytokines, glycolytic rates, and morphological and functional changes in the mitochondria through an mTORC2-dependent, mTORC1-independent mechanism. Leptin also boosts the effects of IL-4 in macrophages, leading to increased oxygen consumption, expression of macrophage markers associated with a tissue repair phenotype, and wound healing. In vivo, hyperleptinemia caused by diet-induced obesity increases the inflammatory response by macrophages. Deletion of leptin receptor and subsequently of leptin signaling in myeloid cells (ObR-/-) is sufficient to improve insulin resistance in obese mice and decrease systemic inflammation. Our results indicate that leptin acts as a systemic nutritional checkpoint to regulate macrophage fitness and contributes to obesity-induced inflammation and insulin resistance. Thus, specific interventions aimed at downstream modulators of leptin signaling may represent new therapeutic targets to treat obesity-induced systemic inflammation. [ABSTRACT FROM AUTHOR]

Published
2022
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results