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• W4385520010 abstract "Abstract Insulin and insulin-like growth factor 1 (IGF-1) are metabolic hormones with known effects on CD4 + T cells through insulin receptor (IR) and IGF-1 receptor (IGF-1R) signaling. Here, we describe specific and distinct roles for these hormones and receptors. We have found that IGF-1R, but not IR, expression is increased following CD4 + T cell activation or following differentiation toward Th17 cells. Although both insulin and IGF-1 increase glycolytic and oxidative metabolism of CD4 + T cells, insulin has a more potent effect. However, IGF-1 has a unique role and acts specifically on Th17 cells to increase IL-17 production and Th17 cell metabolism. Furthermore, IGF-1 decreases mitochondrial membrane potential and mitochondrial reactive oxygen species (mROS) in Th17 cells, providing a cytoprotective effect. Interestingly, both IR and IGF-1R are required for this effect of IGF-1 on mitochondria, which suggests that the hybrid IR/IGF-1R may be required for mediating the effect of IGF-1 on mitochondrial membrane potential and mROS production. Finally, we show that the decrease in mitochondrial membrane potential and mROS caused by IGF-1 is mediated by uncoupling protein 2 (UCP2) activity, and the effects of IGF-1 on CD4 + T cell mitochondria and metabolism are reversed by UCP2 inhibition." @default.
• W4385520010 created "2023-08-04" @default.
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• W4385520010 date "2023-08-03" @default.
• W4385520010 modified "2023-09-27" @default.
• W4385520010 title "Insulin and IGF-1 have both overlapping and distinct effects on CD4+ T cell mitochondria, metabolism, and function" @default.
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• W4385520010 doi "https://doi.org/10.21203/rs.3.rs-3133824/v1" @default.
• W4385520010 hasPublicationYear "2023" @default.
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