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Yinchenhao decoction (YCHD) is a famous traditional Chinese medicine for improving hepatic metabolism disorder. The aim of this study was to investigate the effects of YCHD on lipid metabolism of juvenile largemouth bass fed on high‐carbohydrate diet. Triplicate groups of fish (5.6 ± 0.2 g) were fed six experimental diets (one low‐carbohydrate diet and five high‐carbohydrate diets with gradients YCHD) for 10 weeks. The results showed that appropriate YCHD administration reversed the adverse effects of high‐carbohydrate diet on the growth performance. Meanwhile, YCHD decreased the depositions of hepatic T‐CHO, TG and NEFA, and alleviated lipids deposition in a dose‐dependent manner. Importantly, as the key energy regulating element, AMPK was significantly increased by YCHD, coupled with high expression of β‐oxidation (PPARα and CPT1) and lipids transport (APoB100, MTP, PNPLA7 CD36, CETP and FABP1) genes. Furthermore, PI3K‐AKT pathway was prominently suppressed by YCHD, and the expression of lipids synthesis‐related genes (ACCA, FAS and SCD1) was notably down‐regulated. Additionally, YCHD up‐regulated the expression of glycogen metabolism‐related genes (GSK3β, PGY and GSY). In summary, our results demonstrated that YCHD promoted lipids β‐oxidation and transport, enhanced glucose metabolism and reduced lipids deposition, indicating its beneficial effects on juvenile largemouth bass fed on high‐carbohydrate diet. [ABSTRACT FROM AUTHOR]

Hypoxia is an adverse environmental condition for fish that can have multiple effects. Compared to the natural environment, high-density farming of Schizothorax prenanti is more likely to experience hypoxic conditions. To evaluate the effects of hypoxia, activities of enzymes and expressions of genes that are related to hypoxia responses were measured to understand lipid metabolism, antioxidant capacity, and immnue response changed during hypoxic conditions (dissolved oxygen: 3.0 ± 0.2 mg/L [MHG] and 1.2 ± 0.2 mg/L [SHG]). During hypoxia, the red blood cell content increased. Furthermore, the lactic acid levels in the brain, liver, and muscle increased. Surprisingly, brain Na+/K+-ATPase activity was decreased. Brain and muscle triglyceride (TG) increased at frst, and then decreased, while the nonesterified fatty acids (NEFA) opposite in the brain had the opposite response, Liver TG and NEFA increased during hypoxia. Brain lipoprotein lipase (LPL) activity decreased, but liver and muscle LPL activities and LPL mRNA levels increased during exposure at 0 h and 12 h. Fatty acid binding protein , fatty acid synthase , peroxisome proliferators activated receptor γ coactivator-1α , peroxisome proliferator activated receptors α and γ genes were up-regulated at different time points, especially in SHG. Also, in SHG, malondiadehyde (MDA) levels in the brain and Intestine increased to some extent. Total antioxidative capability (T-AOC) in the brain and muscle tissue decreased, while it increased in gill, Intestine and liver tissue. Catalase (CAT) activity in the brain, gill, Intestine and muscle increased, while it decreased in the liver. Glutathione peroxidase (GSH-Px) activity was decreased in all tissues except brain. The mRNA levels of superoxide dismutase , GSH-Px , CAT , and hypoxia-inducible factor 1 alpha in the brain, gill and liver increased during hypoxia. Tumor necrosis factor , interleukin 1 beta and tropinone reductase-like 22 levels were up-regulated in all tissues, especially in SHG. Also, brain, gill, liver and muscle HSP70 and HSP90 levels increased. In short, hypoxia enhanced lipid metabolism and antioxidant response, and induced up-regulation of antioxidant and immune genes to adapt to environmental hypoxic stress. • Compensatory mechanisms for hypoxia are associated with an increased RBC oxygen transport and energy reallocation. • Hypoxia enhanced lipid metabolism and antioxidant activity. • Hypoxia induced up-regulation of antioxidant and immune genes. [ABSTRACT FROM AUTHOR]