Open AccessImidacloprid Promotes High Fat Diet-Induced Adiposity and Insulin Resistance in Male C57BL/6J Mice
Author(s) -
Quancai Sun,
Xiao Xiao,
Yoo Kim,
Dae-Young Kim,
Kyong Sup Yoon,
J. Marshall Clark,
Yeonhwa Park
Publication year - 2016
Publication title -
journal of agricultural and food chemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.203
H-Index - 297
eISSN - 1520-5118
pISSN - 0021-8561
DOI - 10.1021/acs.jafc.6b04322
Subject(s) - imidacloprid , insulin resistance , adipose tissue , endocrinology , medicine , ampk , white adipose tissue , insulin , biology , adipogenesis , chemistry , protein kinase a , kinase , biochemistry , pesticide , agronomy
Imidacloprid, a neonicotinoid insecticide widely used in agriculture worldwide, has been reported to promote adipogenesis and cause insulin resistance in vitro. The purpose of the current study was to determine the effects of imidacloprid and its interaction with dietary fat in the development of adiposity and insulin resistance using male C57BL/6J mice. Imidacloprid (0.06, 0.6, or 6 mg/kg bw/day) was mixed in a low-fat (4% w/w) or high-fat (20% w/w) diet and given to mice ad libitum for 12 weeks. Imidacloprid significantly promoted high fat diet-induced body weight gain and adiposity. In addition, imidacloprid treatment with the high fat diet resulted in impaired glucose metabolism. Consistently, there were significant effects of imidacloprid on genes regulating lipid and glucose metabolisms, including the AMP-activated protein kinase-α (AMPKα) pathway in white adipose tissue and liver. These results suggest that imidacloprid may potentiate high fat diet-induced adiposity and insulin resistance in male C57BL/6J mice.