Insufficient or Excessive Niacin Intake Induced Glucose and Lipid Metabolic Disorders and Impaired Liver Health in Nile Tilapia

Niacin (vitamin B3) is involved in the metabolic regulation of energy metabolism in animals. However, both deficiency and excess supplementation of niacin can induce profound physiological disturbances in fish. The present study investigated the effect of niacin on energy metabolism and liver health in Nile tilapia (Oreochromis niloticus). Thus, Nile tilapias were fed diets with different niacin supplementation levels (0, 50, 100, and 200 mg/kg) for 8 weeks. The results showed that compared with the niacin-free group, dietary niacin supplementation (50–200 mg/kg) significantly promoted the growth of tilapia. However, excessive niacin supplementation (200 mg/kg) resulted in significantly higher condition factor and viscerosomatic index (VSI) compared to the moderate supplementation groups (50–100 mg/kg). Accordingly, hepatic triglyceride (TG) content was significantly elevated in the excessive niacin group (200 mg/kg). Furthermore, excessive niacin caused hepatic lipid accumulation by enhancing lipogenesis and inhibiting lipid breakdown, as evidenced by the significantly increased the expression of lipogenic genes while suppressing lipolysis and autophagy. Additionally, serum glucose and liver pyruvate in the niacin-free group was significantly lower than in other groups. The key genes of glycolysis and gluconeogenesis were significantly downregulated in the liver of Nile tilapia fed with a niacin-free diet. In contrast, excessive niacin supplementation (200 mg/kg) significantly suppressed hepatic tricarboxylic acid (TCA) cycle-related gene expression, indicating the inhibition of glucose oxidation for energy production. Further analysis of differential metabolites showed that excessive niacin caused accumulation of oxaloacetate, aspartate, and glutathione, but reduced glutamate content. Additionally, tilapia fed with moderate niacin supplementation (50–100 mg/kg) exhibited significantly lower serum alanine aminotransferase enzyme activity compared to both the niacin-free and excessive niacin groups. Hepatic catalase (CAT) and superoxide dismutase (SOD) activities were significantly elevated in this group relative to other groups. Overall, the data suggested that niacin deficiency induced hypoglycemia and reduced glucose activity in Nile tilapia, while excessive niacin led to hepatic lipid accumulation. Both deficient and excessive niacin intake compromised liver health and diminished antioxidant capacity (AOC) in Nile tilapia.