INTESTINAL EFFECTS OF A SUCROSE RICH DIET IN MALE WISTAR RATS

GROMEZ, MALENA; WISZNIEWSKI, MORENA; BORJA, KRISSIA; CYMERYNG, CORA B.; REPETTO, EM

Mar del Plata

Congreso; REUNIÓN CONJUNTA SAIC SAB AAFE AACYTAL 2023; 2023

Sociedad Argentina de Investigación Clínica

In recent years, the obesity epidemic has highlighted the importance of metabolic dysfunction-associated fatty liver disease (MAFLD). We have previously described a model of steatohepatitis associated with insulin-resistance developed in rats by the administration of a sucrose rich diet (SRD). Excessive carbohydrate consumption has been shown to alter the intestinal microbiota and affect intestinal permeability, leading to an increased passage of endotoxins into circulation, primarily reaching the liver. The objective of the current study was to assess the intestinal effects of the SRD. Male Wis- tar rats were divided into two groups: a control diet group (C, n=6) and a group fed 30% sucrose in the drinking water for 12 weeks (SRD, n=6). Fecal samples were collected weekly, and during the 7th week, insulin sensitivity was assessed by an insulin tolerance test. Histological analysis of the ileum showed epithelial changes (hyperplasia), along with a reduced expression of the junction proteins ZO-1 (p<0.05, Mann-Whitney test) and occludin (p=0.05, Mann-Whitney test) by qPCR. Changes in claudin distribution were evaluated by immunofluorescence analysis showing a significance decrease (p<0.001, Student’s t-test). Additionally, significantly high- er levels of circulating endotoxin were observed in SRD-treated rats (p<0.001, Mann-Whitney test). In line with these findings, in the SRD group we also detected an elevated amount of bacterial DNA in the liver (p<0.05, Mann-Whitney test), and a higher Firmicutes/Bacteroidetes ratio, a dysbiosis indicator (by qPCR) in cecal feces from SRD animals was only evident at the 12th week (p<0.001, Mann-Whitney test). In summary, our results indicate that consumption of a high sucrose diet is linked to dysbiosis and disruption of intestinal permeability, potentially fostering an inflammatory process in the liver and exacerbating the effects of insulin resistance in this tissue.