The preferential utilization of hepatic glycogen as energy substrates in largemouth bass (Micropterus salmoides) under short-term starvation

Abstract

To elucidate the underlying mechanism on the energy metabolism in largemouth bass (Micropterus salmoides), cultured sh (initial body weight: 77.57 ± 0.75 g) in the present study were starved for 0 h, 12 h, 24 h, 48 h, 96 h and 192 h, respectively. The proximate composition analysis showed that short-term starvation induced a signi cant up-regulation in crude protein proportion in hepatic of cultured sh (P < 0.05). However, short-term starvation signi cantly decreased the hepatosomatic index and the viscerosomatic index of cultured sh (P < 0.05). The exact hepatic glycogen content in the group starved for 92 h presented remarkable decrease (P < 0.05). Meanwhile, compared with the weight change of lipid and protein (mg) in hepatic (y = 0.0007x 2 -0.2827x + 49.402; y =0.0013x 2 -0.5666x + 165.31), the decreasing trend of weight in glycogen (mg) was more pronounced (y = 0.0032x 2 -1.817x + 326.52), which suggested the preferential utilization of hepatic glycogen as energy substrates under short-term starvation. Gene expression analysis revealed that the starvation down-regulated the expression of insulin-like growth factor 1 and genes of TOR pathway, such as TOR and S6 (P < 0.05). In addition, the starvation signi cantly enhanced expression of lipolysis related genes, including HSL and CPT1, but down-regulated lipogenesis as indicated by the inhibited expression of FAS, ACC1 and ACC2 (P < 0.05). Starvation of 24h upregulated the expression of glycolysis genes, GK, PFKL and PK, and then their expression returned to the normal level. Meanwhile, the expression of gluconeogenesis genes, such as G6PC, FBP1 and PEPCK, was signi cantly inhibited with the short-term starvation (P < 0.05). In conclusion, short-term starvation induced an overall decline in growth performance, but it could deplete the hepatic glycogen accumulation and mobilize glycogen for energy effectively.