MODULATION OF GLUCIDIC PROFILING IN THE INTESTINAL MUCOSA OF THE OBESE ZUCKER RATS

In the intestinal ecosystem, glycoconjugates expressed by the enterocytes and secreted by the goblet cells contribute to the first defensive barrier against pathogenic bacteria and luminal contents. Changes in goblet cell secretion and glycosylation of the intestinal glycocomponents were reported in a variety of intestinal and nutritional disorders and diseases, as well as in conditions requiring total parenteral nutrition. On the other hand, recent findings suggest a possible role for the gut microbiota in obesity and, consequently, in other aspects of metabolic syndrome. Based on these data, the present study was aimed to elucidate the expression and distribution of sialylated and fucosylated glycomponents in the intestinal mucosa of obese Zucker rats (OZR). OZR represent a model of type 2 diabetes exhibiting a moderate degree of arterial hypertension and increased oxidative stress. The occurrence of sialic acids differently linked to D-Gal and/or to D-GalNAc was demonstrated by SNA and MAL II lectin binding. Moreover, additional and complementary data on sialic acid acetylation degree and sites were provided by combining PNA and DBA lectins with chemical and enzymatic pretreatments. Application of LTA, UEA, and AAL lectins allowed to elucidate the fucose profiling in the intestinal epithelium and/or in its secretory products. The binding patterns obtained showed an overall lower intensity of lectin reactivity in OZR compared with control animals. Both sialic acid (a2,6)-D-Gal/D-GalNAc, sialic acid (a2,3)-D-Gal sequences, and fucose residues were affected suggesting possible correlations between the modified glucidic profiling, the obesity condition, and the characteristics of microbial modulation reported in metabolic syndrome.