This leads to insulin resistance and insulin-mediated anti-lipolysis damage, which in turn lead to increased release of circulating fetuin-A from adipose tissue, excessive circulating fetuin-A uptake by the liver, and movement of circulating fetuin-A through the energy sensor AMPK, which is pivotal to directing hepatocytes to potentially deleterious pathways that lead to triglyceridemia [26]. This evidence concerns the gene AHSG and Insulin resistance.