کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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5907535 | 1160025 | 2012 | 4 صفحه PDF | دانلود رایگان |

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.
Journal: Gene - Volume 497, Issue 2, 15 April 2012, Pages 340–343