Glucose homeostasis and glucose tolerance were impaired with elevated lipid to starch ratios in practical diets for the omnivorous genetically improved farmed tilapia Oreochromis niloticus

Abstract

The present study was performed to ascertain if glucose metabolism and glucose tolerance could be regulated by dietary lipid to starch ratios in the omnivorous genetically improved farmed tilapia Oreochromis niloticus. Three isonitrogenous (ca 34.5% protein) and isocaloric (ca 14.5 kJ/g) practical diets were formulated with elevated lipid at the cost of starch provision, being designated as diets L6S23 (5.55% lipid and 22.5% starch), L9S18 (8.77% lipid and 18.1% starch) and L12S13 (12.0% lipid and 13.8% starch). Tilapia juveniles (initial mean body weight: 23.0 g/fish) were allocated to 12 rectangular tanks (250 L) with 20 fish per tank, and were fed experimental diets to apparent satiation for 8 weeks. At the end of the trial, approximately 24 h after the last feeding, fish in each tank were bulk-weighed and counted. Nine fish per tank were sampled to analyze the whole-body composition (3 fish), blood chemistry (3 fish) and the expression of glucose-metabolic genes (3 fish). Thirty-six of the remaining fish per treatment were subjected to an acute glucose tolerance test. The results showed that the growth (weight gain) and feed utilization (feed and protein efficiency ratios) of tilapia were not affected by different treatments. Intraperitoneal fat ratio (1.32%) and lipid percentages in the liver (9.69%) and whole-body (10.2%) of the L12S13 fish were higher than those of the L6S23 fish (0.75%, 6.61% and 8.17%, respectively). The L9S18 (5.24 mmol/L) and L12S13 fish (5.59 mmol/L) obtained higher plasma glucose levels than the L6S23 fish (4.10 mmol/L). In the liver, the mRNA levels of representative genes involved in glycolysis (glucokinase) and glucose release (glucose-6-phosphatase catalytic subunit a2) were simultaneously up-regulated in the L12S13 fish as compared with the L6S23 fish, indicating that a futile cycle between glucose and glucose-6-phosphate was associated with elevated dietary lipid to starch ratios. In the white muscle, the mRNA levels of glucose transporter 1a (glut1a), glut4, hexokinase 1b, phosphofructokinase muscle type a (pfkma), pfkmb and glycogen synthase 1 were 0.44-, 0.71-, 0.58-, 0.51-, 0.72- and 0.53-fold lower in the L12S13 fish than in the L6S23 fish, suggesting that muscular glucose transport and utilization were depressed with elevated dietary lipid to starch ratios. Although it took similar time (3 h) to restore plasma glucose for all treatments, plasma glucose was lower in the L6S23 fish than in the L12S13 fish during 1–3 h after the glucose injection. Additionally, plasma glucose of the L9S18 and L12S13 fish decreased continually along the injection time (during 7–10 h) as compared with the L6S23 fish, which further proved that the regulatory mechanisms of glucose homeostasis were impaired in tilapia that were fed elevated lipid to starch ratios. Our data confirmed that the impairment of glucose homeostasis was also associated with high fat diet reception in the omnivorous tilapia.