Basolateral presence of the proinflammatory cytokine tumor necrosis factor-alpha and secretions from adipocytes and macrophages reduce intestinal sugar transport

Autores: Castilla Madrigal, Rosa María; Gil Iturbe, Eva; Sáinz Amillo, Neira; Moreno Aliaga, María Jesús; Lostao Crespo, María del Pilar (Autor de correspondencia)
ISSN: 0021-9541
Volumen: 234
Número: 4
Páginas: 4352 - 4361
Fecha de publicación: 2019
Lugar: WOS
We have previously demonstrated in Caco-2 cells that tumor necrosis factor-alpha (TNF-alpha) inhibits sugar uptake, acting from the apical membrane, by decreasing the expression of the Na+-glucose cotransporter SGLT1 in the brush border membrane. The goal was to investigate the hypothesis that TNF-alpha from abdominal adipose tissue (adipocytes and macrophages) would decrease sugar and amino acid transport acting from the basolateral membrane of the enterocytes. TNF-alpha placed in the basal compartment of Caco-2 cells decreased alpha-methyl- d-glucose (alphaMG) and glutamine uptake. The apical medium derived from these Caco-2 cells apically placed in another set of cells, also reduced sugar and glutamine transport. Reverse-transcription polymerase chain reaction analysis demonstrated upregulation of TNF-alpha, IL-1beta, and MCP1 expression in Caco-2 cells exposed to basal TNF-alpha. Similarly, MG uptake was inhibited after Caco-2 cells were incubated, in the basal compartment, with medium from visceral human mesenchymal stem cells-derived adipocytes of overweight individuals. The apical medium collected from those Caco-2 cells, and placed in the upper side of other set of cells, also decreased sugar uptake. Basal presence of medium derived from lipopolysaccharide-activated macrophages and nonactivated macrophages decreased MG uptake as well. Diet-induced obese mice showed an increase in the visceral adipose tissue surrounding the intestine.