کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10144534 | 1646303 | 2018 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Impairment of bisphenol F on the glucose metabolism of zebrafish larvae
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کلمات کلیدی
BPABPSPEPCKIRShpfBPFPPARγG6PasePEPCK-CPEPCK-MPI3KDMSO - DMSOinsulin - انسولینinsulin receptor substrate - انسولین بستر گیرندهBisphenol F - بیسفنول Fbisphenol S - بیسفنول SBisphenol A - بیسفنول ای، بیسفنول ADimethyl sulfoxide - دیمتیل سولفواکسیدPhosphatidylinositol 3-kinase - فسفاتیدیلینواستیل 3-کینازphosphoenolpyruvate carboxykinase - فسفوآنولپیرود کربوکسیکینازZebrafish larvae - لاروهای ZebrafishGlucose metabolism - متابولیسم گلوکزAnimal model - مدل حیوانیhexokinase - هگزوکینازpolymerase chain reaction - واکنش زنجیره ای پلیمرازPCR - واکنش زنجیرهٔ پلیمرازpyruvate kinase - پیرووات کینازPeroxisome proliferator-activated receptor gamma - گاما گیرنده گیرنده فعال پرولیفیزوم فعالglucose-6-phosphatase - گلوکز 6-فسفاتازinsulin receptor - گیرنده انسولین
موضوعات مرتبط
علوم زیستی و بیوفناوری
علوم محیط زیست
شیمی زیست محیطی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Bisphenol F (BPF) is a substitute of bisphenol A in the production of epoxy resin and polycarbonate. Its extensive use in consumer products leads to a wide human exposure at high levels. Although the adverse effects of BPF on animal health are of increasing public concern, its risks on systematic glucose metabolism and blood glucose concentrations still remain largely unknown. Using zebrafish larvae as the model animal, we investigated the disturbance of BPF exposure on glucose metabolism and the underlying mechanisms. Zebrafish larvae at 96â¯h post fertilization were exposed to 0.1, 1, 10, and 100â¯Î¼g/L of BPF for 48â¯h. Compared with the control group, glucose levels of larvae increased significantly in the 10 and 100â¯Î¼g/L exposure groups, which are associated with enhancement of gluconeogenesis and suppression of glycolysis induced by high doses of BPF. Additionally, both mRNA expressions and protein levels of insulin increased significantly in the 10 and 100â¯Î¼g/L exposure groups, while transcription levels of genes encoding insulin receptor substrates decreased significantly in these groups, indicating a possibly decreased insulin sensitivity due to impairment of insulin signaling transduction downstream of insulin receptor. Further, compared with BPF alone, co-exposure of larvae to BPF and rosiglitazone, an insulin sensitizer, significantly attenuates increases in both glucose levels and mRNA expressions of a key gluconeogenesis enzyme. Our data therefore indicate impairing insulin signaling transduction may be the main mechanism through which BPF disrupts glucose metabolism and induces hyperglycemia. Results of the present study inform the health risk assessment of BPF and also suggest the use of zebrafish larvae in large-scale screening of chemicals with possible glucose metabolism disturbing effect.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Ecotoxicology and Environmental Safety - Volume 165, 15 December 2018, Pages 386-392
Journal: Ecotoxicology and Environmental Safety - Volume 165, 15 December 2018, Pages 386-392
نویسندگان
Fei Zhao, Hongfang Wang, Penghao Wei, Guobin Jiang, Wei Wang, Xiaona Zhang, Shaoguo Ru,