| First Author | Kiernan K | Year | 2024 |
| Journal | Sci Rep | Volume | 14 |
| Issue | 1 | Pages | 4331 |
| PubMed ID | 38383709 | Mgi Jnum | J:352819 |
| Mgi Id | MGI:7609498 | Doi | 10.1038/s41598-024-54836-w |
| Citation | Kiernan K, et al. (2024) Insulin and IGF-1 have both overlapping and distinct effects on CD4(+) T cell mitochondria, metabolism, and function. Sci Rep 14(1):4331 |
| abstractText | 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 the 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. |
