title: Imidacloprid, a neonicotinoid insecticide, induces insulin resistance.
abstract: Recently, scientific evidence supports a connection between environmental chemical exposures, which includes insecticides, and development of type 2 diabetes. However, there is limited information about the link between influences of neonicotinoid insecticides and incidence of type 2 diabetes. Thus, the purpose of the study was to determine effects of imidacloprid, a neonicotinoid insecticide, on glucose metabolism. Three different cell models were used; adipocytes (3T3-L1), hepatocytes (HepG2), and myotubes (C2C12). These cells were treated with imidacloprid (0, 10, and 20 μM) for 4-6 days followed by treatment with insulin for 15 min to determine responses. Insulin stimulated glucose uptake was reduced by imidacloprid in all three cell culture models. Treatment with imidacloprid reduced phosphorylation of protein kinase B (AKT), one of the major regulators of insulin signaling, without changing overall AKT expression. Subsequently, imidacloprid reduced phosphorylation of ribosomal S6 kinase (S6K), which is a downstream target of AKT and also a feed-back inhibitor of insulin signaling. These results suggest that imidacloprid could induce insulin resistance by affecting the insulin signaling cascade, particularly up-stream of AKT, in adipocytes, liver, and muscle.
authors.affiliation: Department of Food Science, University of Massachusetts, USA.
authors.forename: Jonggun
authors.initials: J
authors.lastname: Kim
authors.forename: Yooheon
authors.initials: Y
authors.lastname: Park
authors.forename: Kyong Sup
authors.initials: KS
authors.lastname: Yoon
authors.forename: J Marshall
authors.initials: JM
authors.lastname: Clark
authors.forename: Yeonhwa
authors.initials: Y
authors.lastname: Park
mesh_terms: D016475:3T3 Cells; D017667:Adipocytes; D000818:Animals; D002478:Cells, Cultured; D003924:Diabetes Mellitus, Type 2 / Q000139:chemically induced / Q000378:metabolism; D005947:Glucose / Q000378:metabolism*; D056945:Hep G2 Cells; D006801:Humans; D007093:Imidazoles / Q000009:adverse effects*; D007306:Insecticides / Q000009:adverse effects*; D007328:Insulin / Q000494:pharmacology / Q000502:physiology*; D007333:Insulin Resistance / Q000235:genetics* / Q000502:physiology; D051379:Mice; D032446:Myoblasts; D000073943:Neonicotinoids; D009574:Nitro Compounds / Q000009:adverse effects*; D010766:Phosphorylation / Q000187:drug effects; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism / Q000502:physiology; D038744:Ribosomal Protein S6 Kinases, 90-kDa / Q000378:metabolism / Q000502:physiology; D015398:Signal Transduction / Q000187:drug effects* / Q000235:genetics*
chemical_list: D007093:Imidazoles; D007306:Insecticides; D007328:Insulin; D000073943:Neonicotinoids; D009574:Nitro Compounds; C082359:imidacloprid; D051057:Proto-Oncogene Proteins c-akt; C069329:RPS6KA1 protein, human; D038744:Ribosomal Protein S6 Kinases, 90-kDa; D005947:Glucose