Antagonistic interaction between perfluorobutanesulfonate and probiotic on lipid and glucose metabolisms in the liver of zebrafish

Perfluorobutanesulfonate (PFBS) and probiotic bacteria can interact to induce hepatic hypertrophy. However, the molecular events occurring in the hypertrophic liver are still unknown. Therefore, we performed this follow-up study using adult zebrafish that were exposed for 40 days to 0 and 10 μg/L PFBS, with or without dietary supplementation of probiotic Lactobacillus rhamnosus. After PFBS or/and probiotic exposures, proteome perturbation, histological pathogenesis and glucose metabolism were investigated in the livers. Proteomic analysis showed potent intervention of PFBS or/and probiotic with hepatic functions. PFBS single exposure caused marked disturbances in lipid metabolisms, which may underlie the severe vacuolization in male liver. The addition of probiotic alleviated the lipid metabolic disorders of PFBS. Furthermore, probiotic supplementation enhanced ATP energy production using glucose in mitochondrial respiratory chain of male fish. However, PFBS alone caused remarkable increase in blood glucose level (by 2.5-fold relative to the control), underlining the onset of hyperglycemia symptom. In contrast, the liver of male fish from the coexposure group functioned appropriately, which immediately increased insulin levels by 2.2-fold to reduce the glucose accumulation in blood. In female liver, PFBS alone significantly decreased the blood glucagon concentration by 2.9-fold. The deficiency of glucagon hormone consequently contributed to the accumulation of glycogen (3.2-fold) therein. Vigorous antagonistic interaction between PFBS and probiotic was noted with respect to glucose metabolism, which restored ATP, glucose, glycogen and glucagon to the control levels. Overall, the present study finds that probiotic L. rhamnosus is efficient to mitigate the metabolic disorders of PFBS on lipid and glucose, highlighting the potential values of probiotic bacteria to protect the aquatic ecosystem. Copyright © 2021 Elsevier B.V. All rights reserved.