INS and Hyperglycemia: A relevant aspect of this pathology is that even before the development of fasting or postprandial hyperglycemia, insulin resistance manifests as abnormalities in triglyceride (TG) storage and lipolysis in insulin-sensitive tissues, causing disruption of insulin signaling, leading to activation of NF-κB and the subsequent upregulation of proinflammatory genes [5, 6].