Figure 6
From: Alteration in kynurenine pathway metabolites in young women with autoimmune thyroiditis
The proposed mechanism links alteration in the kynurenine pathway with disturbances in thyroid function and thyroid homeostasis in young women with autoimmune thyroiditis (AIT). During AIT, the kynurenine pathway of tryptophan metabolism is activated and alteration in this pathway occurs. The formation of AA from KYN is enhanced at the expense of KYNA generation, and at the same time there is a significant reduction in the transformation of AA into 3-HAA. The imbalance between AA and KYNA, reflected by an increase in AA/KYNA ratio and between AA and 3-HAA, resulted in AA accumulation and a slight increase in QA levels. As a consequence of this process, the activity of peripheral deiodinases (SPINA-GD) rose proportionally to AA elevation, which translated into a greater amount of biologically active form of thyroid hormone—FT3. ↑, Increase versus CON, p < 0.05; ↑↑, Increase versus CON, p < 0.01; ↑↑↑, Increase versus CON, p < 0.001; ↓, Decrease versus CON, p < 0.05; p < 0.01; ↓↓↓, Decrease versus CON, p < 0.001. TRP, Tryptophan; TDO, 2,3-Dioxygenase; IDO1, Indoleamine 2,3-dioxygenase; KYN, Kynurenine; KYNU A, Kynureninase A; AA, Anthranilic acid; KMO, Kynurenine 3, Monooxygenase; 3-HKYN, 3-Hydroxykynurenine; KAT, Kynurenine aminotransferase; KYNA, Kynurenic acid; 3-HKYN, 3-Hydroxykynurenine; A3H, Anthranilate-3-hydroxylase; 3-HAA, 3-Hydroxyanthranilic acid; KYNU B, Kynureninase A; 3HAAO, 3-Hydroxyanthranilic acid oxygenase; QA, Quinolinic acid; FT3, Free triiodothyronine.
