IRS-1 (Phospho-Ser312) ELISA Kit

Obesity and type 2 diabetes mellitus have reached an epidemic level, thus novel treatment concepts need to be identified. Myostatin, a myokine known for restraining skeletal muscle growth, has been associated with the development of insulin resistance and type 2 diabetes mellitus. Yet, little is known about the regulation of myostatin in human obesity and insulin resistance. We aimed to investigate the regulation of myostatin in obesity and uncover potential associations between myostatin, metabolic markers and insulin resistance/sensitivity indices. Circulating active myostatin concentration was measured in the serum of twenty-eight severely obese nondiabetic patients compared to a sex and age matched lean and overweight control group (n = 22). Insulin resistance/sensitivity was assessed in the obese group. Skeletal muscle and adipose tissue specimens from the obese group were collected during elective bariatric surgery. Adipose tissue samples from lean and overweight subjects were collected during elective abdominal surgery. Myostatin concentration was increased in obese compared to lean individuals, while myostatin adipose tissue expression did not differ. Muscle myostatin gene expression strongly correlated with expression of metabolic genes such as IRS1, PGC1 alpha, SREBF1. Circulating myostatin concentration correlated positively with insulin resistance indices and negatively with insulin sensitivity indices. The best correlation was obtained for the oral glucose insulin sensitivity index. Our results point to an interesting correlation between myostatin and insulin resistance/sensitivity in humans, and emphasize its need for further evaluation as a pharmacological target in the prevention and treatment of obesity-associated metabolic complications.

Purpose: To investigate the potential role of miR-126 in regulating the proliferation and cisplatin chemosensitivity of human hepatocellular carcinoma (HCC) cells. Methods: The expression of miR-126 was evaluated using clinical HCC specimens. MiR-126-mediated downregulation of Insulin Receptor Substrate 1 (IRS1) was determined by qRT-PCR, western blot and luciferase reporter assay. Cell Counting Kit-8 (CCK8) and colony formation assays were performed to examine the proliferation of HCC cells. Results: Decreased expression of miR126 was found in HCC tumors and was correlated with poor survival in HCC patients. In HCC cells, miR-126 targeted IRS1 for down regulation, through which miR-126 suppressed the growth of HCC cells and desensitized HCC cells to cisplatin treatment. Conclusion: MiR-126a impairs the proliferation and cisplatin chemoresistance of HCC cells by targeting IRS1.