Abstract

This study was performed to investigate the time course of changes in the expression of preproinsulin (ins) and insulin-degrading enzyme (ide), plasma insulin level and hepatic glucose metabolism after a glucose tolerance test (GTT) in genetically improved farmed Nile tilapia (GIFT), Oreochromis niloticus. Male adult fish were intraperitoneally injected with 1g glucose/kg of body weight after 24h of food deprivation, and then subjected to sampling at 0, 1, 2, 4, 6 and 12h after the GTT. Compared with the control (4.3mM/L), plasma glucose level peaked at 1h (14.8mM/L), decreased during 2–4h (5.7–8.3mM/L), and was restored after 6h of the GTT. Although the expression of ins1, ins2 and ide were not affected in the Brockman body, plasma insulin level concomitantly increased with the increase of plasma glucose level during 1–4h after the glucose injection. The expression of glucose transporter 1 sharply increased at 1h after the GTT, indicating that hepatic glucose uptake was stimulated. The mRNA level of glucokinase was up-regulated during 1–4h, and the activity of phosphofructokinase increased during 2–4h, suggesting that hepatic glycolysis was active during 1–4h after the glucose administration. The mRNA level of glycogen synthase 1 increased at 1h, and liver glycogen level accumulated at 4h after the GTT. Although the expression of glucose-6-phosphatase catalytic subunit a2 was suppressed during 1–2h, neither the mRNA level of phosphoenolpyruvate carboxykinase 2 nor its activity was impacted by the glucose injection, which might have prolonged the glucose clearance of tilapia. Hepatic lipogenesis was effectively stimulated to dispose excess glucose absorbed by the hepatocytes, as up-regulation of mRNA levels of ATP citrate lyase a (during 1–4h), acetyl-CoA carboxylase α (during 4–12h) and fatty acid synthase (during 2–12h) were accompanied by the GTT. Taken together, it was concluded that glucose was an effective insulin secretagogue in tilapia, and liver played an important role to clear the glucose load through stimulation of glucose uptake, glycolysis, glycogenesis and lipogenesis.

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