Postprandial regulation of glucose metabolism and insulin signaling pathways in Macrobrachium rosenbergii

Abstract

To better understand postprandial glucose metabolic mechanisms in crustaceans, the pathways involved in glucose transport, breakdown, synthesis, and regulation were investigated in the giant freshwater prawn Macrobrachium rosenbergii after feeding. Prawns were fasted for 48 hours and then refed to satiation. Glucose and glycogen contents, along with the transcriptional levels of glucose metabolism-related genes, were measured at 0, 1, 3, 6, and 10 hours after feeding (HAF). Plasma glucose levels peaked at 3 HAF and returned to basal levels by 6–10 HAF. Hepatopancreas glucose followed a similar trend, except for a notable increase at 10 HAF, suggesting gluconeogenesis at this time point. Expression analysis of glucose transporter genes in hepatopancreas revealed a significant upregulation of GLUT1 at 3, 6, and 10 HAF, while GLUT2 showed significant decreases only at 6 HAF. Glycolysis-related genes (GK and PK) exhibited transient increases post-feeding, whereas the gluconeogenesis-related gene FBP was initially suppressed, with expression recovering from 6 HAF onward. The glycogenesis-related gene GS was significantly upregulated at 3, 6, and 10 HAF, correlating with increased glycogen levels in the hepatopancreas. Conversely, the expression of the glycogenolysis-related gene GDE was inhibited after feeding, along with a decrease in the glycogenesis inhibitory gene GSK3. Genes in the insulin signaling pathway (ILP, PI3KCa, and AKT) were upregulated post-feeding, peaking at 3 HAF and subsequently declining. These results suggest that feeding stimulates the insulin signaling pathway and GLUT1 to transport excess glucose, inducing glycolysis and hepatopancreatic glycogenesis, while inhibiting gluconeogenesis and glycogenolysis.

Keywords

• Postprandial metabolism
• Glucose
• Insulin signaling pathway
• Macrobrachium rosenbergii