Transforming growth factor beta-like stimulated clone 22 D4 promotes diabetic hyperglycemia and insulin resistance [abdominal fat]

ABSTRACT: Obesity-related insulin resistance represents the core component of the so-called Metabolic Syndrome, ultimately promoting glucose intolerance, pancreatic beta cell failure, and overt type 2 diabetes 1 2. Based on substantial side effects of existing pharmacological approaches, efficient and safe insulin sensitization and glucose control remain critical therapeutic aims to prevent diabetic late complications 3. Here, we identify Transforming Growth Factor beta-like Stimulated Clone (TSC) 22 D4 as a critical molecular determinant of insulin signaling and glucose handling. Hepatocyte-specific inactivation of TSC22D4 enhanced insulin signaling in liver and skeletal muscle, while hepatic TSC22D4 overexpression blunted insulin tissue responses. Consequently, hepatic TSC22D4 inhibition both prev

ORGANISM(S): Mus musculus

SUBMITTER: Carsten Sticht 

PROVIDER: E-GEOD-53753 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress