GEO DataSets

(Submitter supplied) Branched-chain amino acids (BCAA) have emerged as predictors of type 2 diabetes (T2D). However, their potential role in the pathogenesis of insulin resistance and T2D remains unclear. By integrating data from skeletal muscle gene expression and metabolomic analyses, we demonstrate evidence for perturbation in BCAA metabolism and fatty acid oxidation in skeletal muscle from insulin-resistant humans. Experimental modulation of BCAA flux in cultured cells alters fatty acid oxidation in parallel. Furthermore, heterozygosity for the BCAA metabolic enzyme methylmalonyl-CoA mutase (MUT) alters muscle lipid metabolism in vivo, resulting in increased muscle triacylglycerol (TAG) accumulation and increased body weight after high-fat feeding. Together, our results demonstrate that impaired muscle BCAA catabolism may contribute to the development of insulin resistance by reducing fatty acid oxidation and increasing TAG accumulation.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL1261

10 Samples

Download data: CEL, CHP

(Submitter supplied) Insulin resistance in skeletal muscle is a key phenotype associated with type 2 diabetes (T2D) and is even present in offspring of diabetic parents. However, molecular mediators of insulin resistance remain unclear. We find that the top-ranking gene set in expression analysis of muscle from humans with T2D and normoglycemic insulin resistant subjects with parental family history (FH+) of T2D is increased expression of actin cytoskeleton genes regulated by serum response factor (SRF) and its coactivator MKL1. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Dataset:

GDS3884

Platform:

GPL570

50 Samples

Download data: CEL

Analysis of quadriceps muscle from type 2 diabetes (T2D) patients and from normoglycemic but insulin-resistant subjects with a parental family history of T2D. Insulin resistance in skeletal muscle is a key phenotype of T2D. Results provide insight into the molecular basis of this insulin resistance.

Organism:

Homo sapiens

Type:

Expression profiling by array, count, 3 disease state, 2 gender sets

Platform:

GPL570

Series:

GSE25462

50 Samples

Download data: CEL