ArticleMolecular metabolism2026
Insulin resistance induced by pesticides is overcome by pancreatic islet adaptation in a mouse model of Parkinson's disease.
Article in Molecular metabolism, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Exposure to certain pesticides appears to be involved in type 2 diabetes and Parkinson's disease onset which are reported to be epidemiologically associated. While the exact causes of this association and the deleterious mechanisms linking these aging-associated diseases are not fully known, it seems important to assess the extent to which environmental factors such as pesticides could be involved. Our aim was to evaluate the consequences of chronic dietary exposure to a mixture of pesticides at levels below the Acceptable Daily Intake in transgenic mice predisposed to develop motor disorders. Male mice expressing mutated A53T human α-synuclein (M83) and wild-type mice were fed either a control or a diet enriched with 6 pesticides (captan, boscalid, chlorpyrifos, thiachloprid, thiofanate, ziram) for 50 weeks. Exposure to pesticides led to body weight gain and insulin resistance in wild-type and M83 mice, caused, at least in part, by a reduction in insulin receptor levels in liver, skeletal muscle and adipose tissue. However, only M83 mice exposed to pesticides showed early motor deficits associated with decreased insulin receptor levels in midbrain and striatum. While pesticides promoted glucose intolerance in wild-type mice, M83 mice surprisingly showed improved glucose tolerance accompanied by a significant increase in pancreatic beta-cell mass and function. Transcriptomic analysis further revealed an enrichment of genes involved in amino-acid metabolism in M83 mouse islets with abundant α-synuclein expression. Overall, exposure to pesticides led to insulin resistance, which can be overcome thanks to a previously unrecognized role of α-synuclein in beta-cell adaptation.
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