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Pancreas Development and Nutrient Uptake and Utilization Are Disrupted by Embryonic Exposures to the Environmental Toxicant Perfluorooctanesulfonic Acid in the Zebrafish
Author(s) -
Sant Karilyn E,
Jacobs Haydee M,
Borofski Katrina A,
Chen Phoebe,
Park Yeonhwa,
TimmeLaragy Alicia R
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.792.8
Subject(s) - biology , yolk , embryonic stem cell , pancreas , embryogenesis , toxicant , proteases , embryo , population , zebrafish , medicine , endocrine system , andrology , endocrinology , microbiology and biotechnology , biochemistry , toxicity , hormone , gene , food science , enzyme , demography , sociology
Several persistent and ubiquitous environmental toxicants have been categorized as diabetogens or obesogens due to their numerous associations with these conditions in adult humans. These compounds often produce deleterious effects in the pancreas, which secretes glucoregulatory hormones and proteases and lipases essential for digestion. Compounds such as the surfactant perfluorooctanesulfonic acid (PFOS) have been detected in biological samples from nearly 100% of the population, and are associated with increased risk for diabetes in adults. However, the developmental consequences of these exposures which may contribute to these adult phenotypes require elucidation. We hypothesized that embryonic exposures to PFOS would alter pancreas development and disrupt embryonic nutrition processes associated with pancreas function. Zebrafish embryos were exposed to 16 or 32 μM PFOS or 0.01% DMSO (control) throughout embryonic development (3–96 hpf). Transgenic embryos from Tg(insulin:GFP) and Tg(ptf1a:GFP) strains were imaged in vivo at 96 hpf to visualize endocrine and exocrine pancreatic development, respectively. Larval morphometry was examined to probe yolk utilization and fish growth. RNA was isolated to examine expression of genes central to pancreas function, and biochemical assays were performed to quantify total embryonic nutrient concentrations. Beta cell mass and insulin gene expression were both decreased concordantly with increasing PFOS exposure at 96 hpf. Total pancreas length and expression of protease genes were also decreased by PFOS exposure. The rate of yolk utilization was increased by 6–10% due to 16 and 32 μM PFOS, respectively, suggesting increased embryonic uptake of total yolk nutrients. However, total embryonic concentrations of the bulk yolk nutrients cholesterol, triglycerides, and glucose were decreased with increasing PFOS concentrations. These PFOS‐exposed larvae were also shorter than control fish at 7 dpf. Free fatty acid profiles also differed between control and PFOS‐exposed embryos. Total embryonic concentrations of several saturated free fatty acids such as stearic acid were increased by treatment, while concentrations of beneficial unsaturated free fatty acids such as α‐linolenic acid were decreased by treatment. Overall, this work demonstrates that embryonic toxicant exposures can perturb pancreas development, and can alter the uptake and processing of yolk nutrients during development. Support or Funding Information This work was supported in part by the National Institutes of Health (R01 ES025748 to ART‐L), and a University of Massachusetts Amherst Commonwealth Honors College Research grant (to KAB.).