Imidacloprid Promotes High Fat Diet-Induced Adiposity and Insulin Resistance in Male C57BL/6J Mice.

TitleImidacloprid Promotes High Fat Diet-Induced Adiposity and Insulin Resistance in Male C57BL/6J Mice.
Publication TypeJournal Article
Year of Publication2016
AuthorsSun, Q, Xiao, X, Kim, Y, Kim, D, Yoon, KSup, Clark, JM, Park, Y
JournalJ Agric Food Chem
Date Published2016 Dec 14
KeywordsAdipose Tissue, White, Adiposity, AMP-Activated Protein Kinases, Animals, Blood Glucose, Diet, High-Fat, Humans, Imidazoles, Insecticides, Insulin, Insulin Resistance, Liver, Male, Mice, Mice, Inbred C57BL, Neonicotinoids, Nitro Compounds, Obesity, Weight Gain

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.

Alternate JournalJ Agric Food Chem
PubMed ID27960282
PubMed Central IDPMC5325319
Grant ListR21 ES023128 / ES / NIEHS NIH HHS / United States