Effects of heat shock treatment on glucose metabolism in grass carp (Ctenopharyngodon idellus) juveniles.

摘要

Fish species have poor capability of carbohydrate metabolism relative to mammals. Specifically, fish cannot utilize dietary glucose well. Heat shock protein 72 (Hsp72) can be induced by heat shock and prevent stress-induced activation of c-Jun amino N-terminal kinase (JNK) which then promotes the insulin signaling pathway in mammals. However, the function of Hsp72 on glucose utilization is unknown in fish. We conducted a study to understand the role played by heat shock on glucose utilization using juveniles of the grass carp fish. In this study, the juveniles of grass carp were fed with either high glucose diet or control diet. Half of the juveniles were subjected to several temporary heat shock treatments within 8 weeks. The growth performance, body composition of juveniles and the expression of glucose metabolism related genes, including Hsp72 in the livers of juveniles were analyzed from each group. The heat shock treatments could improve growth performance and body composition of grass carp juveniles, and could activate JNK. Though the expression of Hsp72 increased significantly in Group GH (juveniles fed with high-glucose diet and given heat shock treatment) (P<0.05) as measured by fluorescent real time PCR and Western blot, the expression of JNK and p-JNK were not suppressed by Hsp72 in our study, which was different from some previous studies in mammals. In summary, the study showed that heat shock did not affect glucose metabolism through JNK pathway in grass carp. This may give a clue to explain why fish species have a much poorer capability of carbohydrate metabolism than mammals.