The effect of curcumin on PI3K/Akt and AMPK pathways in insulin resistance induced by fructose

Abstract Objectives Excessive fructose consumption is recognized to elevate insulin resistance in animals and humans. In our study, we aimed to assess the possible consequences of curcumin (curc) treatment applied to rat models of fructose-induced insulin resistance on adenosine monophosphate-activated protein kinase (AMPK) and phosphatidylinositol-3 kinase (PI3K)/protein kinase B (Akt) pathways in skeletal muscle and adipose tissue. Methods We established four distinct rat groups: corn oil (negative control group), 20 % fructose (positive control group), 20 % fructose and 100 mg/kg curc (100 mg/kg curc group), and 20 % fructose and 200 mg/kg curc (200 mg/kg curc group). The ELISA method was used to determine serum insulin levels, an auto-analyzer was used to measure serum glucose levels, and homeostatic model assessment of insulin resistance (HOMA-IR) values were calculated. In the rat’s skeletal muscle and adipose tissues, the ELISA method was used to determine the following parameters: insulin receptor substrate-1 (IRS-1), phosphorylated insulin receptor substrate-1 (p-IRS-1), PI3K, phosphatidylinositol 3,4,5-trisphosphate (PIP3), phosphoinositide-dependent kinases (PDK-1), phosphorylated Akt (p-Akt), AMPK and glucose transporter type 4 (GLUT4) levels. Results The positive control group exhibited a significant increase in serum glucose, insulin, and HOMA-IR levels, confirming the establishment of the insulin resistance model. In the curcumin dose groups, these values significantly decreased. Additionally, compared to the positive control groups, curcumin dose groups demonstrated a significant increase in the parameters of the Akt/PI3K pathway, AMPK activation, and GLUT4 levels in skeletal muscle and adipose tissues. Conclusions We observed that curcumin demonstrates potential ameliorative effects on the insulin signaling pathway through PI3K/Akt and AMPK pathways.