RT Journal Article
T1 Metabolic endotoxemia promotes adipose dysfunction and inflammation in human obesity.
A1 Clemente-Postigo, Mercedes
A1 Oliva-Olivera, Wilfredo
A1 Coin-Aragüez, Leticia
A1 Ramos-Molina, Bruno
A1 Giraldez-Perez, Rosa María
A1 Lhamyani, Said
A1 Alcaide-Torres, Juan
A1 Perez-Martinez, Pablo
A1 El Bekay, Rajaa
A1 Cardona, Fernando
A1 Tinahones, Francisco J
K1 fatty acid binding protein
K1 human adipose tissue
K1 human obesity
K1 leptin
K1 lipopolysaccharides
AB Impaired adipose tissue (AT) lipid handling and inflammation is associated with obesity-related metabolic diseases. Circulating lipopolysaccharides (LPSs) from gut microbiota (metabolic endotoxemia), proposed as a triggering factor for the low-grade inflammation in obesity, might also be responsible for AT dysfunction. Nevertheless, this hypothesis has not been explored in human obesity. To analyze the relationship between metabolic endotoxemia and AT markers for lipogenesis, lipid handling, and inflammation in human obesity, 33 patients with obesity scheduled for surgery were recruited and classified according to their LPS levels. Visceral and subcutaneous AT gene and protein expression were analyzed and adipocyte and AT in vitro assays performed. Subjects with obesity with a high degree of metabolic endotoxemia had lower expression of key genes for AT function and lipogenesis ( SREBP1, FABP4, FASN, and LEP) but higher expression of inflammatory genes in visceral and subcutaneous AT than subjects with low LPS levels. In vitro experiments corroborated that LPS are responsible for adipocyte and AT inflammation and downregulation of PPARG, SCD, FABP4, and LEP expression and LEP secretion. Thus, metabolic endotoxemia influences AT physiology in human obesity by decreasing the expression of factors involved in AT lipid handling and function as well as by increasing inflammation.
YR 2018
FD 2018-11-13
LK http://hdl.handle.net/10668/13178
UL http://hdl.handle.net/10668/13178
LA en
DS RISalud
RD Apr 13, 2025