Abstract
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-deficient 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.
Copyright © 2012 Elsevier B.V. All rights reserved.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Animals
-
Diabetes Mellitus, Experimental / genetics*
-
Diabetes Mellitus, Experimental / metabolism*
-
Diet, High-Fat / methods
-
Glucose Transporter Type 2 / genetics
-
Glucose Transporter Type 2 / metabolism
-
Glucose-6-Phosphatase / genetics
-
Glucose-6-Phosphatase / metabolism
-
Liver / metabolism
-
Male
-
Mice
-
Mice, Inbred C57BL
-
Myeloid Differentiation Factor 88 / deficiency
-
Myeloid Differentiation Factor 88 / genetics*
-
Myeloid Differentiation Factor 88 / metabolism*
-
Obesity / metabolism
-
Stearoyl-CoA Desaturase / genetics*
-
Stearoyl-CoA Desaturase / metabolism*
Substances
-
Glucose Transporter Type 2
-
Myd88 protein, mouse
-
Myeloid Differentiation Factor 88
-
Slc2a2 protein, mouse
-
Scd1 protein, mouse
-
Stearoyl-CoA Desaturase
-
Glucose-6-Phosphatase