T1D commonly develops in children not consuming alcohol themselves. Even in case this disease is manifests during adolescence of adulthood, the initiation of the disease process conceivably occurred before the age of alcohol introduction. Obviously, we are not proposing alcohol to be used as a prophylactic treatment against T1D. Nevertheless, mechanistically the findings are of interest. Indeed, Tubacin in another autoimmune disorder, rheumatoid arthritis, mainly occurring in adults, alcohol has been associated with a decreased risk of developing the disease. The similarity indices between DGGE profiles based on caecum samples collected from the animals at the time of diagnosed diabetes or at the end of the study indicates that the administration of alcohol at the age of 6 weeks, does not change the composition of the gut microbiota significantly at the time of sample collection. The decreased diabetic incidence cannot be directly referred to a difference in the overall composition of the gut microbiota between the animals. Since ethanol does not facilitate insulin sensitivity in rats, but rather induces the opposite, we doubt that the beneficial effect of ethanol has metabolic causes,TWS119 for example by inducing a relative beta-cell rest. Considering an immunological mechanism modulated by ethanol seems therefore to be more pertinent. Diabetes is significantly reduced or delayed by increase of regulator CD4+CD25+ T cells or NKT cells. In NOD mice, the low level of NKT cells in particular seems to be of interest. Also, patients developing T1D were shown to display low NKT cell levels. NKT cells are induced by stimulation with glycolipids presented by CD1d molecules. Interestingly, CD1d knock-out NOD mice show an exacerbation of diabetes, whereas upregulation of CD1d expression within the beta cells restores the immune regularity function of NKT cells preventing diabetes. In two mice strains the levels of some glycosphingolipids in pancreas have been examined: sulfatide is significantly more present in NOD compared to BALB/c mice, and sulfated lactosyl ceramide is expressed in NOD mice only. We favour the interpretation that alcohol results in improved glycolipid loading to CD1d and signalling to NKT cells, affecting development of experimental autoimmune diabetes.