Reduced fatty acid β-oxidation improves glucose catabolism and liver health in Nile tilapia (Oreochromis niloticus) juveniles fed a high-starch diet

2021 
Abstract Fish are poor users of dietary carbohydrates and often display prolonged hyperglycemia and fat deposition after feeding high digestible carbohydrate diets. Recently, fatty acid β-oxidation (FAO) inhibition has been reported to increase glucose oxidation in fish. Therefore, this study tested the assumption that the inhibition of FAO with mildronate (MD, a carnitine synthesis inhibitor) might also increase glucose utilization and alleviate adverse effects induced by high starch diet (HSD) in Nile tilapia, Oreochromis niloticus. Nile tilapia juveniles (6.13 ± 0.11 g) were cultured in nine 200-L tanks (30 fish per tank) and divided into three groups (three tanks per group). The fish were fed twice a day (9:00 and 18:30) at 4% body weight by using a normal starch diet (NSD, 30% corn starch), a HSD (45% corn starch), or a HSD supplemented with MD (25 g/kg of diet, HSD + MD) for eight weeks. These three feeds contained approximately 35.8% protein and 6.4% lipid. The fish each tank were weighed every two weeks, and the feeding amount was adjusted accordingly. After the feeding trial, the fish fed on HSD showed higher hepatosomatic index (HSI), visceral somatic index (VSI), serum triglyceride concentration and whole-body and tissue (liver and muscle) lipid contents than those fed on NSD. The fish fed on HSD also had higher relative area of vacuolation in the liver, hepatic malondialdehyde (MDA) content, and aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities in the serum than those fed on NSD. Moreover, the fish fed on HSD increased serum glucose and insulin concentrations, and hepatic lactate, pyruvate and glycogen contents, but reduced whole-body protein content and dietary protein utilization than those fed on NSD, indicating that HSD induced fat deposition, liver damage, glucose intolerance and lowered protein-sparing effect. However, the fish fed on HSD + MD decreased hepatic carnitine content and FAO activity, attenuated the indexes related to fat deposition and liver damage, improved blood glucose clearance and whole-body protein deposition than those fed on HSD, suggesting that the adverse effects caused by HSD were reversed after FAO inhibition. Furthermore, the fish fed on HSD down-regulated the expression of genes associated with glucose uptake, glycolysis, FAO process, and lipolysis compared to those fed on HSD + MD and NSD, yet up-regulated lipogenic and proteolytic genes. These data suggested that inhibition of FAO improved glucose utilization and alleviated the HSD-induced adverse effects in Nile tilapia. This work demonstrates that, modifying mitochondrial FAO activity regulates the ability of fish to adapt to HSD intake through remodeling energy homeostasis. Our study provides new insights into improving carbohydrate utilization in aquatic animals.
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