Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
5907535 | Gene | 2012 | 4 Pages |
Saturated fatty acids, acting as ligands for toll-like receptor 4 (TLR4), induce inflammation and mediate the development of insulin resistance. Myeloid differentiation factor 88 (MyD88) is an adaptor protein for TLR4. Previously, we found MyD88-deificient mice fed a high-fat diet (HFD) exhibited a severe diabetic phenotype. Stearoyl-CoA Desaturase 1 (SCD1) is the rate-limiting enzyme in the biosynthesis of monounsaturated fatty acids and known as a risk factor of diabetes. In the present study, we found SCD1 was dramatically increased in HFD-fed MyD88-deficient mice liver. This finding showed the novel linkage between MyD88 and SCD1 in the development of diabetes mellitus.
► We investigated mechanisms of diabetes observed in MyD88-deificient mice fed a HFD. ► MyD88-deficiency did not affect expression levels of G6Pase. ► MyD88-deficiency did not affect expression levels of GLUT2. ► SCD1 was up-regulated on the liver samples of MyD88-deificient mice fed a HFD. ► These results suggest MyD88 and SCD1 would link for the development of diabetes.