| Title: | Chronic low-dose exposure to imidacloprid potentiates high fat diet-mediated liver steatosis in C57BL/6J male mice |
| Authors: | Nimako, Collins Browse this author |
| Ikenaka, Yoshinori Browse this author →KAKEN DB |
| Okamatsu-Ogura, Yuko Browse this author →KAKEN DB |
| Bariuan, Jussiaea V Browse this author |
| Kobayashi, Atsushi Browse this author |
| Yamazaki, Ryo Browse this author |
| Taira, Kumiko Browse this author |
| Hoshi, Nobuhiko Browse this author |
| Hirano, Tetsushi Browse this author |
| Nakayama, Shouta M. M. Browse this author →KAKEN DB |
| Ishizuka, Mayumi Browse this author →KAKEN DB |
| Keywords: | neonicotinoid insecticides |
| imidacloprid |
| liver steatosis |
| no observable adverse effect level (NOAEL) |
| Issue Date: | Mar-2021 |
| Publisher: | 公益社団法人 日本獣医学会 (The Japanese Society of Veterinary Science) |
| Journal Title: | Journal of veterinary medical science |
| Volume: | 83 |
| Issue: | 3 |
| Start Page: | 487 |
| End Page: | 500 |
| Publisher DOI: | 10.1292/jvms.20-0479 |
| Abstract: | Hepatic steatosis is known to precede a continuum of events that lead to hepatic metabolic dysfunction, inflammation and carcinogenesis. Recently, studies have linked xenobiotic exposures to hepatic steatogenesis and its associated metabolic disorders; however, the underlying mechanisms remain elusive. This study aimed to elucidate the mechanistic role of imidacloprid in the prevalence of high fat diet (HFD)-induced liver steatosis, using a C57BL/6J mice model. Mice (3 weeks old) were fed with HFD and treated with 0.6 mg/kg bw/day (one-tenth of the NOAEL) of imidacloprid through water or diet, for 24 weeks. In a controlled group, mice were fed with only HFD. At the end of the study, imidacloprid treatment significantly potentiated HFD-induced body weight gain in mice. Also, imidacloprid increased the liver weights of mice, with complimentary reductions in mesenteric and gonadal white adipose tissue weights. Histopathological analysis of liver revealed a drastic steatosis in imidacloprid treated mice. Following a real-time qPCR analysis, imidacloprid upregulated transcriptions of hepatic fatty acid biosynthesis-related transcription factors and genes. Imidacloprid also induced hepatic expression of the gene encoding pregnane X receptor; but had no significant effect on hepatic expressions of liver X receptor and aryl hydrocarbon receptor. The imidacloprid treatment further enhanced serum alanine aminotransferase levels but downregulated hepatic antioxidant mRNA expressions. Ultimately, this study suggested an imidacloprid-potentiation effects on prevalence of HFD-induced liver steatosis via transcriptional modulations of the hepatic FA biosynthesis pathway. |
| Type: | article |
| URI: | http://hdl.handle.net/2115/82023 |
| Appears in Collections: | 獣医学院・獣医学研究院 (Graduate School of Veterinary Medicine / Faculty of Veterinary Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)
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