Endocr Pract. 2020 Jan;26(1):82-96. doi: 10.4158/EP-2019-0162. Epub 2019 Sep 26.
Autoimmune thyroid disease, including Graves disease (GD) and Hashimoto thyroiditis (HT), is one of the most common endocrine diseases. GD and HT are the main etiologies for hyperthyroidism and hypothyroidism, respectively. This study aimed to provide a metabolomic analysis of GD patients with hyperthyroidism and HT patients with hypothyroidism. This study investigated serum metabolomics in 43 GD patients with hyperthyroidism, 45 HT patients with hypothyroidism, and 52 age- and sex-matched healthy controls. The metabolomic data were analyzed by performing multivariate statistical analysis. The 186 metabolites including amino acids, bile acids, free fatty acids, and lipids were identified in all participants. Multivariate models indicated systematic differences in the hyperthyroidism, hypothyroidism, and control groups. Compared to healthy controls, the 22 metabolites in the hyperthyroidism group and the 17 metabolites in the hypothyroidism group were significantly changed. Pathway analysis showed that hyperthyroidism had a significant impact on arginine and proline metabolism and aminoacyl-transfer ribonucleic acid biosynthesis, while hypothyroidism had a significant impact on alanine, aspartate, and glutamate metabolism. The serum metabolomic pattern changes in patients with autoimmune thyroid dysfunction. = body mass index; = cholic acid; = chenodeoxycholic acid; = deoxycholic acid; = fasting plasma glucose; = fasting plasma insulin; = free triiodothyronine; = free thyroxine; = Graves disease; = glycodeoxycholic acid; = high-density lipoprotein cholesterol; = homeostasis model assessment of insulin resistance; = Hashimoto thyroiditis; = low-density lipoprotein cholesterol; = phosphatidylcholine; = principal component analysis; = partial least squares discriminant analysis; = sphingomyelin; = total bile acid; = total cholesterol; = triglyceride; = thyrotropin; = variable influences on projection.
自身免疫性甲状腺疾病包括格雷夫斯病（GD）和桥本甲状腺炎（HT），是最常见的内分泌疾病之一。GD 和 HT 分别是甲亢和甲减的主要病因。本研究旨在对 GD 甲亢患者和 HT 甲减患者进行代谢组学分析。
该研究纳入了 43 例 GD 甲亢患者、45 例 HT 甲减患者和 52 名年龄和性别匹配的健康对照者，对其血清代谢组学进行了研究。采用多元统计分析对代谢组学数据进行了分析。
在所有参与者中，共鉴定出包括氨基酸、胆汁酸、游离脂肪酸和脂质在内的 186 种代谢物。多元模型表明，甲亢组、甲减组和对照组之间存在系统差异。与健康对照组相比，甲亢组的 22 种代谢物和甲减组的 17 种代谢物发生了显著变化。通路分析显示，甲亢对精氨酸和脯氨酸代谢及氨酰基转移核糖核酸合成有显著影响，而甲减对丙氨酸、天冬氨酸和谷氨酸代谢有显著影响。
自身免疫性甲状腺功能障碍患者的血清代谢组学模式发生改变。
= 体重指数；= 胆酸；= 鹅脱氧胆酸；= 去氧胆酸；= 空腹血糖；= 空腹胰岛素；= 游离三碘甲状腺原氨酸；= 游离甲状腺素；= 格雷夫斯病；= 甘氨脱氧胆酸；= 高密度脂蛋白胆固醇；= 胰岛素抵抗评估的稳态模型；= 桥本甲状腺炎；= 低密度脂蛋白胆固醇；= 磷脂酰胆碱；= 主成分分析；= 偏最小二乘判别分析；= 鞘磷脂；= 总胆汁酸；= 总胆固醇；= 甘油三酯；= 促甲状腺激素；= 投影变量影响。
