Bisphenol A induces hepatic triglyceride level in adult male rare minnow Gobiocypris rarus

Bisphenol A (BPA), an endocrine disruptor, exist in almost all waters. In the present study, we expose adult male Gobiocypris rarus rare minnow to 15 mu g/L BPA to study the effect BPA on fish hepatic lipid metabolism. Following 1, 3 and 5 weeks exposure, the liver tissue of rare minnow was separated. The change of the hepatic morphology, hepatosomatic index, lipid composition and expression of lipid metabolism related genes were analyzed through paraffin section, oil red O staining, lipidomic analysis, and quantitative real-time PCR. BPA can cause significant hepatic lipid deposition in male rare minnow, leading to an increase in triglyceride (TG) level (1.84-22.87-fold), but it is also accompanied by a decrease in diglyceride level (1.67-4.78-fold). The expression of lipid metabolism related genes showed that BPA exposure can up-regulate TG synthesis related genes expression, and down-regulate TG degradation genes expression. Expression of TG transport related genes were also disrupted by BPA. It suggests that BPA can up-regulate rare minnow hepatic TG level through multi-path, and ultimately lead to lipid accumulation in the liver. The results of the present study enrich the mechanisms of environmental endocrine disruptors affecting lipid accumulation in fish.

Automated summary

The study showed that BPA exposure significantly increased hepatic lipid deposition in male rare minnow, with an increase in triglyceride level and a decrease in diglyceride level. The expression of lipid metabolism related genes indicated that BPA up-regulates TG synthesis related genes expression and down-regulates TG degradation genes expression, disrupting TG transport related genes as well. Overall, the study enriches the understanding of how environmental endocrine disruptors like BPA affect lipid accumulation in fish.