Exposure to permethrin promotes high fat diet-induced weight gain and insulin resistance in male C57BL/6J mice

Permethrin is a pyrethroid pesticide that was previously reported to promote fat accumulation and insulin resistance in vitro. A recent study in female mice also found that permethrin could promote high fat-induced insulin resistance. The effects of permethrin on glucose and lipid metabolisms in mal...

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Veröffentlicht in:Food and chemical toxicology 2018-01, Vol.111, p.405-416
Hauptverfasser: Xiao, Xiao, Sun, Quancai, Kim, Yoo, Yang, Szu-Hao, Qi, Weipeng, Kim, Daeyoung, Yoon, Kyong Sup, Clark, John M., Park, Yeonhwa
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Sprache:eng
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Zusammenfassung:Permethrin is a pyrethroid pesticide that was previously reported to promote fat accumulation and insulin resistance in vitro. A recent study in female mice also found that permethrin could promote high fat-induced insulin resistance. The effects of permethrin on glucose and lipid metabolisms in male mice, however, remain unknown. The purpose of this study was to investigate the effects and interactions of permethrin exposure (50, 500, and 5000 μg/kg body weight/day) and dietary fat (low fat, 4% w/w; high fat, 20% w/w) on development of obesity and insulin resistance in male C57BL/6J mice. Our results showed that permethrin treatment significantly increased body weight, fat mass, and insulin resistance with high fat diet, but not with low fat diet, without influencing energy intake. Permethrin treatment also significantly increased serum levels of insulin, glucose, leptin, triglycerides and cholesterol. Further results showed that permethrin inhibited AMP-activated protein kinase in white adipose tissue. These results suggest that permethrin interacts with dietary fat to alter lipid and glucose metabolisms in male C57BL/6J mice. •Permethrin promoted high fat diet-induced insulin resistance in male mice.•Permethrin promoted high fat diet-induced weight and fat mass gain in male mice.•Permethrin inhibited AMP-activated protein kinase in white adipose tissue.
ISSN:0278-6915
1873-6351
DOI:10.1016/j.fct.2017.11.047