AKT1 and Insulin resistance: Furthermore, FNCF‐treated cell supernatants induced hepatic insulin resistance by upregulating extracellular signal‐regulated kinase (ERK) phosphorylation, which subsequently disrupted the insulin receptor substrate 1 (IRS1)/protein kinase B (AKT)/glycogen synthase kinase 3β (GSK3β) pathway, impairing glycogen synthesis in hepatocytes.70