Chronic low-dose exposure to imidacloprid potentiates high fat diet-mediated liver steatosis in C57BL/6J male mice
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.
| Medienart: |
E-Artikel |
|---|
| Erscheinungsjahr: |
2021 |
|---|---|
| Erschienen: |
2021 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:83 |
|---|---|
| Enthalten in: |
The Journal of veterinary medical science - 83(2021), 3 vom: 03. Apr., Seite 487-500 |
| Sprache: |
Englisch |
|---|
| Beteiligte Personen: |
Nimako, Collins [VerfasserIn] |
|---|
| Links: |
|---|
| Themen: |
3BN7M937V8 |
|---|
| Anmerkungen: |
Date Completed 28.07.2021 Date Revised 02.01.2024 published: Print-Electronic Citation Status MEDLINE |
|---|
| doi: |
10.1292/jvms.20-0479 |
|---|
| funding: |
|
|---|---|
| Förderinstitution / Projekttitel: |
|
| PPN (Katalog-ID): |
NLM320497267 |
|---|
| LEADER | 01000caa a22002652 4500 | ||
|---|---|---|---|
| 001 | NLM320497267 | ||
| 003 | DE-627 | ||
| 005 | 20240108140551.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 231225s2021 xx |||||o 00| ||eng c | ||
| 024 | 7 | |a 10.1292/jvms.20-0479 |2 doi | |
| 028 | 5 | 2 | |a pubmed24n1246.xml |
| 035 | |a (DE-627)NLM320497267 | ||
| 035 | |a (NLM)33487623 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 100 | 1 | |a Nimako, Collins |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Chronic low-dose exposure to imidacloprid potentiates high fat diet-mediated liver steatosis in C57BL/6J male mice |
| 264 | 1 | |c 2021 | |
| 336 | |a Text |b txt |2 rdacontent | ||
| 337 | |a ƒaComputermedien |b c |2 rdamedia | ||
| 338 | |a ƒa Online-Ressource |b cr |2 rdacarrier | ||
| 500 | |a Date Completed 28.07.2021 | ||
| 500 | |a Date Revised 02.01.2024 | ||
| 500 | |a published: Print-Electronic | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a 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 | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a imidacloprid | |
| 650 | 4 | |a liver steatosis | |
| 650 | 4 | |a neonicotinoid insecticides | |
| 650 | 4 | |a no observable adverse effect level (NOAEL) | |
| 650 | 7 | |a Neonicotinoids |2 NLM | |
| 650 | 7 | |a Nitro Compounds |2 NLM | |
| 650 | 7 | |a imidacloprid |2 NLM | |
| 650 | 7 | |a 3BN7M937V8 |2 NLM | |
| 700 | 1 | |a Ikenaka, Yoshinori |e verfasserin |4 aut | |
| 700 | 1 | |a Okamatsu-Ogura, Yuko |e verfasserin |4 aut | |
| 700 | 1 | |a Bariuan, Jussiaea V |e verfasserin |4 aut | |
| 700 | 1 | |a Kobayashi, Atsushi |e verfasserin |4 aut | |
| 700 | 1 | |a Yamazaki, Ryo |e verfasserin |4 aut | |
| 700 | 1 | |a Taira, Kumiko |e verfasserin |4 aut | |
| 700 | 1 | |a Hoshi, Nobuhiko |e verfasserin |4 aut | |
| 700 | 1 | |a Hirano, Tetsushi |e verfasserin |4 aut | |
| 700 | 1 | |a Nakayama, Shouta M M |e verfasserin |4 aut | |
| 700 | 1 | |a Ishizuka, Mayumi |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |t The Journal of veterinary medical science |d 1997 |g 83(2021), 3 vom: 03. Apr., Seite 487-500 |w (DE-627)NLM012627488 |x 1347-7439 |7 nnns |
| 773 | 1 | 8 | |g volume:83 |g year:2021 |g number:3 |g day:03 |g month:04 |g pages:487-500 |
| 856 | 4 | 0 | |u http://dx.doi.org/10.1292/jvms.20-0479 |3 Volltext |
| 912 | |a GBV_USEFLAG_A | ||
| 912 | |a GBV_NLM | ||
| 951 | |a AR | ||
| 952 | |d 83 |j 2021 |e 3 |b 03 |c 04 |h 487-500 | ||