Gangliosides and GDNF pathway in diabetic small intestine

SÁNCHEZ M. N.; HONORÉ S. M.; GENTA S. B.; SÁNCHEZ S. S.

Mar del Plata. Buenos Aires. Argentina

Congreso; XLIII Annual Meeting of the Argentine Society for Biochemistry and Molecular Biology (SAIB); 2007

Society for Biochemistry and Molecular Biology (SAIB)

Chronic diabetes give arise to multiple complication including those of gastrointestinal tract. Diabetic intestinal motility dysfunction is associated with pathological lesions that occur in the enteric neurons. However the mechanisms underlying these changes in the enteric nervous system are not well defined. Gangliosides (Gls), sialic acid-containing glicoesphingolipids are present at cell surface. Recent studies indicate that they are implicated in many biological functions including cell-cell interaction, cell activation, and signal transduction through modulation of growth factors. In addition Gls play role in neuron survival and death. In this study we investigated the pattern of Gls and GDNF/GFRá1-Ret signal pathway in the small intestine of diabetic mice. Samples were analyzed by TUNEL, immunohistochemistry, thin layer chromatography and RT-PCR. A significantly increase of apoptotic cells was observed at the myenteric plexus level of diabetic animals. Also we observed quantitative and qualitative changes  in the pattern of intestinal Gls. Diabetes produces a significant decrease in GD1a, GD3, GM1 and an increase expression of GM3. Semi-quantitative variations on GDNF/GFRá1-Ret mRNA levels were observed under diabetic state. In conclusion we suggest that the impairment of enteric neurons could be mediated by alterations in both GLs pattern and in consonance with GDNF pathway.