Insulin and IGF-1 have both overlapping and distinct effects on CD4+ T cell mitochondria, metabolism, and function.

Autor:	Kiernan, Kaitlin, Alwarawrah, Yazan, Nichols, Amanda G., Danzaki, Keiko, MacIver, Nancie J.
Předmět:	T cells CYTOPROTECTION T helper cells SOMATOMEDIN C HORMONE receptors METABOLISM MEMBRANE potential INSULIN receptors
Zdroj:	Scientific Reports; 2/21/2024, Vol. 14 Issue 1, p1-11, 11p
Abstrakt:	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. [ABSTRACT FROM AUTHOR]
Databáze:	Complementary Index
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