Abstract
Sentinel species such as the Atlantic killifish (Fundulus heteroclitus) living in urban waterways can be used as toxicological models to understand impacts of environmental metabolism disrupting compound (MDC) exposure on both wildlife and humans. Exposure to MDCs is associated with increased risk of metabolic syndrome, including impaired lipid and glucose homeostasis, adipogenesis, appetite control, and basal metabolism. MDCs are ubiquitous in the environment, including in aquatic environments. New Bedford Harbor (NBH), Massachusetts is polluted with polychlorinated biphenyls (PCBs), and, as we show for the first time, tin (Sn). PCBs and organotins are ligands for two receptor systems known to regulate lipid homeostasis, the aryl hydrocarbon receptor (AHR) and the peroxisome proliferator-activated receptors (PPARs), respectively. In the current study, we compared lipid homeostasis in laboratory-reared killifish from NBH (F2) and a reference location (Scorton Creek, Massachusetts; F1 and F2) to evaluate how adaptation to local conditions may influence responses to MDCs. Adult killifish from each population were exposed to 3,3′,4,4′,5-pentachlorobiphenyl (PCB126, dioxin-like), 2,2′,4,4′,5,5′-hexachlorobiphenyl (PCB153, non-dioxin-like), or tributyltin (TBT, a PPARγ ligand) by a single intraperitoneal injection and analyzed after 3 days. AHR activation was assessed by measuring cyp1a mRNA expression. Lipid homeostasis was evaluated phenotypically by measuring liver triglycerides and organosomatic indices, and at the molecular level by measuring the mRNA expression of pparg and ppara and a target gene for each receptor. Acute MDC exposure did not affect phenotypic outcomes. However, overall NBH killifish had higher liver triglycerides and adiposomatic indices than SC killifish. Both season and population were significant predictors of the lipid phenotype. Acute MDC exposure altered hepatic gene expression only in male killifish from SC. PCB126 exposure induced cyp1a and pparg, whereas PCB153 exposure induced ppara. TBT exposure did not induce ppar-dependent pathways. Comparison of lipid homeostasis in two killifish populations extends our understanding of how MDCs act on fish and provides a basis to infer adaptive benefits of these differences in the wild.
Highlights
The dramatic rise in obesity worldwide has drawn considerable clinical and research attention
This study evaluated the effects of acute exposure to metabolism disrupting compound (MDC) on lipid homeostasis in adult killifish at the phenotypic and molecular levels
Condition factor was calculated for killifish in all but the first experiment, in which standard length and resected organ weights were not recorded at euthanasia
Summary
The dramatic rise in obesity worldwide has drawn considerable clinical and research attention. One conclusion from obesity-related research is that diet and exercise cannot entirely explain the global obesity epidemic. A complex array of genetic, epigenetic, environmental and behavioral factors contribute to an individual’s risk of obesity (e.g., Burgio et al, 2015). This discovery has led to the identification of environmental metabolism disrupting compounds (MDCs), a class of compounds that alter metabolic homeostasis, including lipid and glucose homeostasis, adipogenesis, appetite control, and basal metabolism (e.g., Grün & Blumberg, 2006, 2009; Heindel et al, 2017). Among MDCs are pollutants common in aquatic environments such as organotins (e.g., tributyltin, TBT; Grün and Blumberg, 2006; Heindel et al, 2017) and dioxin- and nondioxin-like polychlorinated biphenyls (PCBs; Baker et al, 2013; Gadupudi et al, 2015; Wahlang et al, 2013)
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
