Glycometabolic disorder induced by chronic exposure to low-concentration imidacloprid in zebrafish.

ABSTRACT

The health risks induced by chronic exposure to low concentrations of imidacloprid (IMI) to zebrafish were investigated in this study. The results indicated that the growth of zebrafish was inhibited after being exposed to 10, 100, and 500 µg/L of IMI for 90 days. Moreover, the blood glucose levels in the IMI-exposed groups were significantly higher compared to the control group. Investigation into the development of zebrafish larvae revealed that IMI exposure hindered the development of the liver and pancreatic islets, organs crucial for glucose metabolism. In addition, the IMI-exposed groups exhibited reduced liver glycogen and plasma insulin levels, along with changes in the activity of enzymes and the transcription levels of genes associated with liver glucose metabolism. These findings suggest that IMI induces glycometabolic disorders in zebrafish. The analysis of intestinal flora revealed that several key bacteria associated with an elevated risk of diabetes were significantly altered in IMI-exposed fish. Specifically, a remarkable decrease was found in the abundance of the genera Aeromonas and Shewanella, which have been found closely related to the development of pancreatic islets. This implies that the alteration of key bacteria in the fish gut by IMI, which in turn affects the development of organs such as the pancreatic islets, may be the initial trigger for abnormalities in glucose metabolism. Our results revealed that chronic exposure to low concentrations of IMI led to glycometabolic disorder in fish. Therefore, considering the pervasive existence of IMI residues in the environment, the health hazards posed by low-concentration IMI to fish cannot be overlooked.