Many fish species experience natural periods of starvation; however, mobilization of energy sources may vary. To elucidate the mechanism underlying energy utilization and metabolic adaptation to food deprivation in gibel carp (Carassis auratus gibelio var. CAS III), fish (initial body weight 111.13 +/- 0.65 g) were starved for 0 d, 1 d, 2 d, 7 d, and 21 d, respectively. After seven days of food deprivation, plasma glucose levels significantly decreased, whereas plasma free fatty acids levels significantly increased. Liver glycogen levels in the group starved for 7 d significantly decreased, whereas muscle glycogen levels decreased in the group starved for 21 d, suggesting that glycogen in the liver is first utilized to provide energy than glycogen in the muscle. The transcriptional levels of glucose transporter type 2 (GLUT2) in the liver were upregulated during starvation. No changes in the mRNA levels of glycolytic enzymes such as glucokinase (GK) and 6-phosphofructokinase (6PFK) were observed in the liver. Gluconeogenic potential increased with starvation, possibly for blood glucose homeostasis, as indicated by the enhanced mRNA levels of gluconeogenic enzymes, including glucose-6-phosphatase (G6Pase), fructose 1,6-bisphosphatase (FBPase), and phosphoenolpyruvate carboxykinase (PEPCK). The observation of a decrease in liver triglycerides content and the enhanced expression of hormone-sensitive lipase (HSL) and lipoprotein lipase (LPL) suggests the mobilization of lipid reserve in the liver. Enhanced fatty acid oxidation as indicated by the upregulated mRNA carnitine palmitoyl transferase 1 isoform a (CPT1a) and acyl-CoA oxidase 3 (ACO3) levels in the liver suggests that fatty acids are catabolized to provide energy during starvation. Sterol regulatory element binding protein 1 (SREBP1), ATP citrate lyase (ACLY), acetyl-CoA carboxylase (ACC), and fatty acid synthase (FAS) were downregulated during starvation in both liver and muscle, indicating suppressed lipogenesis.