Dietary supplementation with a PPARγ agonist promotes adipocyte hyperplasia and improves high-fat diet tolerance and utilization in grass carp (Ctenopharyngodon idellus)

Due to the wide usage of high-fat diets in aquaculture, improving the ability of fish to utilize high-fat diets is one of the important issues in the field of aquaculture nutrition. Studies in mammals have proven that increasing the number of adipocytes improves high-fat diet-induced metabolic disease, suggesting that promoting adipocyte hyperplasia has potential as a novel nutritional strategy to reverse the negative effects of high-fat diets in farmed fish. To verify this hypothesis, a total of 270 juvenile grass carp (Ctenopharyngodon idellus) (34.57 ± 0.29 g) were randomly divided into 15 net cages, and a PPARγ agonist (rosiglitazone) was added to the high-fat diet to promote PPARγ-mediated adipocyte hyperplasia. The results showed that PPARγ was activated in adipose tissue instead of the liver and muscle, resulting in adipogenesis and healthy adipose tissue remodeling, including an increased ability to store and metabolize fat and decreased lipid accumulation, immune cell penetration and fibrosis, as well as inflammation. In addition, promoting PPARγ-mediated adipocyte hyperplasia significantly reduced the levels of inflammation in serum, liver and muscle (P < 0.05) and significantly reduced the serum contents of total triglycerides, total cholesterol, aspartate aminotransferase and alanine aminotransferase (P < 0.05), indicating that the tolerance of grass carp to high-fat diets was increased. Subsequently, the growth performance and feed efficiency were significantly improved. Meanwhile, hepatic steatosis decreased as a result of reduced lipid absorption and synthesis, and the synthesis of protein in muscle was significantly increased by promoting the ability of muscle to utilize fat. Taken together, activating PPARγ-mediated adipocyte hyperplasia not only increases the tolerance of grass carp to high-fat diets but also promotes the utilization of high-fat diets and increases the protein-sparing effect of fat in grass carp. Our study indicates that targeting PPARγ-mediated adipocyte hyperplasia to change the pattern of adipose tissue expansion is a nutritional strategy to develop feed additives, which are used to reverse the negative effects of high-fat diets and promote the utilization of high-fat diets in farmed fish.