It had been suggested that chronic exposure to Schistosoma mansoni prevents the onset of Th1-mediated diseases such as diabetes mellitus. The present study was carried out on four groups of mice: (1) control group, (2) group infected with S. mansoni, (3) group injected with streptozotocin to induce diabetes, and (4) group infected and then 3 months postinfection injected with streptozotocin. No differences were detected between the infected non-diabetic and infected diabetic groups regarding worm burden, tissue egg count, and oogram. At the same time, results showed a reducing effect of S. mansoni infection on the rate of glucose uptake by the diaphragm with reduction in glycogen content of soleus muscle. This an important issue since skeletal muscle is the primary site for insulin-stimulated glucose disposal. In conclusion, because of the detected depressed peripheral glucose uptake by the diaphragm, the protecting effect of helminths infection in diabetes should be reconsidered, to be able to devise therapeutic strategies for the treatment of autoimmune diseases.