Is the Immunogenic Action of Gluten Enough to Aggravate Obesity in Non-coeliac Individuals?

Abstract

The pathogenesis of obesity involves a chronic low-grade inflammation. Gluten has been involved in rupture of intestinal barrier, disorganization of the intestinal junction complex and changes in intestinal microbiota. These actions favor the absorption of immunogenic components (such as LPS and several gliadin derivate peptides) to the submucosa and intensify the chronic low-grade inflammation seen in obesity.

In mice, gluten intake was associated to down regulation of proteins involved on browning process, reduction of thermogenesis and increase of pro-inflammatory cytokine expression in adipose tissue. Nevertheless, other studies showed that gluten-free diets were associated to nutrient unbalance, obesogenic microbiota profile and metabolic syndrome.

Despite the growing number of in vitro and experimental evidences suggesting that gluten could facilitate the development of obesity by inducing inflammation and altering energetic metabolism, no consensus has been established. Obesity is the result of a complex interaction of nutrients that act favoring or preventing the expansion of adipose tissue. Despite our knowledge about the immunogenic role of gluten, until controlled clinical studies confirm (or deny) the efficacy of GFD on weight loss, positions in favor or against gluten-free diet to treat or to prevent obesity are merely speculative.