Obesity and Lipodystrophy Center, Endocrinology Unit, University Hospital of Pisa, Pisa, Italy.
Department of Clinical and Experimental Medicine, University Hospital of Pisa, Via Paradisa 2, 56124, Pisa, Italy.
J Endocrinol Invest. 2022 Feb;45(2):413-423. doi: 10.1007/s40618-021-01662-w. Epub 2021 Aug 15.
Subjects with obesity may exhibit an increase in serum TSH concentrations. Several mechanisms have been proposed to explain this association, including the presence of a compensatory mechanism to counterbalance an accelerated turnover of thyroid hormones in subjects with obesity. This study aimed at evaluating whether the thyroids of subjects with obesity differs from those of normal-weight individuals regarding histology and gene expression profiling.
Ninety-eight patients were selected among those scheduled for thyroidectomy. At histology, thyroid tissue samples were investigated for the presence of adipocytes and/or lymphocyte infiltration. In a subset of patients, the expression at mRNA level of several genes involved in metabolic pathways and immune cell-related mechanisms was quantified by NanoString Technology.
The presence of adipose cells was documented in thyroid specimens from 40% normal weight, 52.9% overweight and 73.5% patients with obesity. The number of infiltrating adipocytes was greater in specimens of patients with overweight or obesity compared to normal weight. The lymphocytes common antigen (CD45) and mast cell (MC) scores, and the number of CD3+ and CD8+ lymphocytes were higher in patients with overweight and obesity than in normal-weight subjects. Several genes involved in metabolic pathways were differently expressed in patients with overweight or obesity compared to normal weight, with upregulation of Leptin receptor and downregulation of Fatty Acid-Binding Protein 5.
Increased BMI is associated with adipocyte and lymphocyte infiltration of the thyroid, not related to an autoimmune process, which might affect thyroid function in subjects with obesity. A differential gene expression profiling of metabolic and immune pathways in thyroid tissues of patients with obesity was also observed.
肥胖症患者可能会出现血清 TSH 浓度升高。有几种机制被提出解释这种关联,包括在肥胖症患者中存在一种补偿机制来抵消甲状腺激素的加速代谢。本研究旨在评估肥胖症患者的甲状腺在组织学和基因表达谱方面是否与正常体重个体有所不同。
从计划接受甲状腺切除术的患者中选择了 98 例患者。在组织学方面,研究了甲状腺组织样本中是否存在脂肪细胞和/或淋巴细胞浸润。在部分患者中,通过 NanoString 技术定量测定了几个涉及代谢途径和免疫细胞相关机制的基因的 mRNA 水平表达。
在 40%的正常体重、52.9%的超重和 73.5%的肥胖患者的甲状腺标本中发现了脂肪细胞。与正常体重患者相比,超重或肥胖患者的甲状腺标本中浸润的脂肪细胞数量更多。淋巴细胞共同抗原(CD45)和肥大细胞(MC)评分以及 CD3+和 CD8+淋巴细胞的数量在超重和肥胖患者中高于正常体重患者。与正常体重患者相比,超重或肥胖患者中几个涉及代谢途径的基因表达不同,瘦素受体上调,脂肪结合蛋白 5 下调。
BMI 的增加与甲状腺中的脂肪细胞和淋巴细胞浸润有关,与自身免疫过程无关,这可能会影响肥胖症患者的甲状腺功能。还观察到肥胖症患者甲状腺组织中代谢和免疫途径的差异基因表达谱。