title: A review on the molecular mechanisms involved in insulin resistance induced by organophosphorus pesticides.
abstract: There is increasing evidence reporting that organophosphorus pesticides (OPs) impair glucose homeostasis and cause insulin resistance and type 2 diabetes. Insulin resistance is a complex metabolic disorder that defies explanation by a single etiological pathway. Formation of advanced glycation end products, accumulation of lipid metabolites, activation of inflammatory pathways and oxidative stress have all been implicated in the pathogenesis of insulin resistance. Ultimately, these molecular processes activate a series of stress pathways involving a family of serine kinases, which in turn have a negative effect on insulin signaling. Experimental and clinical data suggest an association between these molecular mechanisms and OPs compounds. It was first reported that OPs induce hyperglycemia. Then a concomitant increase of blood glucose and insulin was pointed out. For some years only, we have begun to understand that OPs promote insulin resistance and increase the risk of type 2 diabetes. Overall, this review outlines various mechanisms that lead to the development of insulin resistance by OPs exposure.
authors.affiliation: Laboratory of Aggression Physiology and Endocrine Metabolic Studies, Department of Biology, Faculty of Sciences, Tunis, Tunisia. Electronic address: lasram_montassar@yahoo.fr.
authors.forename: Mohamed Montassar
authors.initials: MM
authors.lastname: Lasram
authors.affiliation: Laboratory of Aggression Physiology and Endocrine Metabolic Studies, Department of Biology, Faculty of Sciences, Tunis, Tunisia.
authors.forename: Ines Bini
authors.initials: IB
authors.lastname: Dhouib
authors.affiliation: Laboratory of Aggression Physiology and Endocrine Metabolic Studies, Department of Biology, Faculty of Sciences, Tunis, Tunisia.
authors.forename: Alya
authors.initials: A
authors.lastname: Annabi
authors.affiliation: Laboratory of Aggression Physiology and Endocrine Metabolic Studies, Department of Biology, Faculty of Sciences, Tunis, Tunisia. Electronic address: salouaelfazaa@tunet.tn.
authors.forename: Saloua
authors.initials: S
authors.lastname: El Fazaa
authors.affiliation: Laboratory of Aggression Physiology and Endocrine Metabolic Studies, Department of Biology, Faculty of Sciences, Tunis, Tunisia. Electronic address: najoua.gharbi@planet.tn.
authors.forename: Najoua
authors.initials: N
authors.lastname: Gharbi
mesh_terms: D000818:Animals; D005947:Glucose / Q000378:metabolism / Q000502:physiology; D006801:Humans; D007249:Inflammation / Q000139:chemically induced / Q000473:pathology; D007333:Insulin Resistance / Q000235:genetics* / Q000502:physiology*; D050356:Lipid Metabolism / Q000187:drug effects; D009765:Obesity / Q000235:genetics / Q000503:physiopathology; D009943:Organophosphorus Compounds / Q000633:toxicity*; D018384:Oxidative Stress / Q000187:drug effects; D010575:Pesticides / Q000633:toxicity*; D015398:Signal Transduction / Q000187:drug effects
chemical_list: D009943:Organophosphorus Compounds; D010575:Pesticides; D005947:Glucose
keywords: Glucotoxicity; Inflammation; Insulin resistance; Lipotoxicity; Organophosphorus; Oxidative stress