Department of Translational Research and New Technologies in Medicine and Surgery, University of Pisa, Via Savi 10, Pisa, 56126, Italy.
Department of Clinical and Experimental Medicine, University of Pisa, School of Medicine, Via Savi, 10, I-56126, Pisa, Italy.
Rev Endocr Metab Disord. 2018 Dec;19(4):349-354. doi: 10.1007/s11154-018-9477-9.
Myo-inositol (Myo-Ins) plays an important role in thyroid function and autoimmunity. Myo-Ins is the precursor for the synthesis of phosphoinositides, which takes part in the phosphatidylinositol (PtdIns) signal transduction pathway, and plays a decisive role in several cellular processes. In the thyroid cells, PtdIns is involved in the intracellular thyroid-stimulating hormone (TSH) signaling, via Phosphatidylinositol (3,4,5)-trisphosphate (PtdIns(3,4,5)P3) (PIP-3). Moreover, the phosphatidyl inositol 3 kinases (PI3K) family of lipid kinases regulates diverse aspects of T, B, and Tregs lymphocyte behaviour. Different mouse models deficient for the molecules involved in the PIP3 pathway suggest that impairment of PIP3 signaling leads to dysregulation of immune responses and, sometimes, autoimmunity. Studies have shown that cytokines modulate Myo-Ins in thyroid cells. Moreover, clinical studies have shown that after treatment with Myo-inositol plus seleniomethionine (Myo-Ins + Se), TSH levels significantly declined in patients with subclinical hypothyroidism due to autoimmune thyroiditis. The treatment was accompanied by a decline of antithyroid autoantibodies. After treatment serum CXCL10 levels declined, confirming the immune-modulatory effect of Myo-Ins. Additional research is necessary in larger population to evaluate the effect on the quality of life, and to study the mechanism of the effect on chemokines.
肌醇（Myo-Ins）在甲状腺功能和自身免疫中起着重要作用。Myo-Ins 是合成磷脂酰肌醇（PtdIns）的前体，参与磷脂酰肌醇（PtdIns）信号转导途径，在几个细胞过程中起决定性作用。在甲状腺细胞中，PtdIns 通过磷酸肌醇（3,4,5）三磷酸（PtdIns（3,4,5）P3）（PIP-3）参与细胞内促甲状腺激素（TSH）信号转导。此外，磷脂酰肌醇 3 激酶（PI3K）家族的脂质激酶调节 T、B 和 Treg 淋巴细胞行为的各个方面。涉及 PIP3 途径的分子缺陷的不同小鼠模型表明，PIP3 信号转导的损伤导致免疫反应失调，有时导致自身免疫。研究表明细胞因子可调节甲状腺细胞中的 Myo-Ins。此外，临床研究表明，在自身免疫性甲状腺炎引起的亚临床甲状腺功能减退症患者中，用肌醇加硒甲硫氨酸（Myo-Ins+Se）治疗后，TSH 水平显著下降。治疗伴随着甲状腺自身抗体的下降。治疗后血清 CXCL10 水平下降，证实了 Myo-Ins 的免疫调节作用。需要在更大的人群中进行更多的研究，以评估对生活质量的影响，并研究对趋化因子影响的机制。
