Functional Characterization of the PI3K/AKT Pathway in Glucose Metabolism of Macrobrachium rosenbergii

The glucose intolerance of the crustacean limits its carbohydrate utilization, and the underlying metabolic mechanisms remain poorly understood. While the PI3K/AKT pathway is a central regulator of insulin-mediated glucose metabolism in vertebrates, its role in crustacean is largely unexplored. This study investigated the function of the PI3K/AKT pathway in glucose metabolism in the giant freshwater prawn, Macrobrachium rosenbergii. Prawns were injected with the PI3K-specific inhibitor LY294002 or a PBS control, followed by a glucose tolerance test. Western blot analysis confirmed that LY294002 significantly inhibited AKT phosphorylation in hemocytes. Inhibition of the PI3K/AKT pathway resulted in impaired glucose clearance, evidenced by significantly higher plasma glucose and trehalose levels post-glucose injection. Concurrently, hepatopancreatic glycogen and triglyceride contents were significantly reduced in the inhibitor group. Gene expression analysis revealed that PI3K inhibition inhibited the glucose-induced upregulation of genes involved in glycolysis, glycogenesis, and lipogenesis in hepatopancreas. This study provides the first direct functional evidence supporting the conserved role of PI3K/AKT pathway in carbohydrate metabolism in M. rosenbergii, providing preliminary knowledge for understanding glucose intolerance of crustacean.