Lead induced disorders of lipid metabolism and glycometabolism in the liver of developmental Japanese quails (Coturnix japonica) via inhibiting PI3K/Akt signaling pathway

The lead (Pb) contamination is considered a lethal threat to birds. However, Pb-induced hepatotoxicology especially its impacts on metabolic processes in the liver of birds is not yet fully understood. Therefore, we tried to determine the toxicological effects of Pb exposure on hepatic carbohydrate and lipid metabolism via Phos-phatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) pathway by using an animal model-Japanese quail (Coturnix japonica). One-week old female Japanese quails were randomly allocated into four groups and fed with 0, 50 ppm, 500 ppm and 1000 ppm Pb drinking water respectively for 49 days. The results showed that Pb accumulated in the liver as a dose-dependent manner. Exposure to high dose of Pb (500 and 1000 ppm Pb) led to severe histopathological damages characterized by irregularity and dilation of liver sinusoids, hepatic lipid vacuolization and hepatocellular cytoplasm hyalinization. Meanwhile, Pb exposure caused glycogen increase and lipid droplets decrease in the liver. Pb exposure was also attributable to a decreased triglyceride level in the plasma. In addition, the transcriptional levels of PI3K and Akt in the liver were downregulated by Pb exposure. Subsequently, the mRNA expressions of genes related with glycometabolism in the liver were remarkably altered and the mRNA levels of genes involved in fat synthesis and oxidation in the liver were also markedly changed. it seems that Pb could lead to liver metabolic disorder through structural damages and PI3K/Akt signaling pathway disruption.

Automated summary

This study investigated the toxicological effects of lead exposure on hepatic carbohydrate and lipid metabolism in birds. Using the Japanese quail as an animal model, the study found that lead accumulation in the liver was dose-dependent. High dose exposure to lead caused severe histopathological damages and disruption of the PI3K/Akt signaling pathway. Furthermore, lead exposure altered the expression of genes related to glycometabolism, fat synthesis, and oxidation in the liver, leading to liver metabolic disorder.