Kar Kaushik, Sinha Satwika
Associate Professor, Department of Biochemistry, Calcutta National Medical College, Kolkata, West Bengal, India.
Assistant Professor, Department of Biochemistry, Calcutta National Medical College, Kolkata, West Bengal, India.
J Clin Diagn Res. 2017 Aug;11(8):BC07-BC09. doi: 10.7860/JCDR/2017/26666.10345. Epub 2017 Aug 1.
Hypothyroidism is a common concern in endocrinology practice, which plays a significant role in metabolic and development processes. Obesity, hyperlipidaemia and hypertension may complicate hypothyroidism. Recent studies have shown that cytokines like leptin and adiponectin, secreted by adipose tissue and exert their endocrinal functions by modulating appetite, obesity and insulin sensitivity in conjunction with thyroid hormones. Interrelation between thyroid hormone, insulin resistance and adipokines are not yet clear.
To estimate serum leptin, adiponectin and insulin resistance in patients with hypothyroidism and to compare with control subjects and measure the relation between the mean value of one variable with others.
Forty primary hypothyroidism patients and forty age and sex matched controls were selected for the study with informed consent. Fasting serum Thyroid Stimulating Hormone (TSH), leptin, adiponectin, glucose and insulin were estimated. Homeostatic Model Assessment of Insulin Resistance (HOMA-IR) was evaluated from fasting plasma glucose and serum insulin levels. Statistical analysis was carried out using SPSS version 17.0. Unpaired t-test and regression analysis were used to compare and determine the dependence, p<0.05 was considered significant.
Serum TSH, leptin, adiponectin HOMA-IR were significantly higher (p<0.05) in patients with hypothyroidism (10.37±4.10, 10.97±0.60, 31.09±4.07, 3.64±0.40) than controls (2.41±2.09, 10.37±0.12, 33.32±1.44, 2.36±0.35). Regression analysis showed that leptin was significantly (p=0.054) dependent on adiponectin but not on others.
Increased oxidative stress by hypothyroid mediated leptin secretion and increased insulin resistance can down-regulate the adiponectin secretion and future complications. Serum estimation and correction of imbalance of adipokines in hypothyroidism can prevent severe consequences.
甲状腺功能减退是内分泌科临床常见问题,在代谢和发育过程中起重要作用。肥胖、高脂血症和高血压可能使甲状腺功能减退复杂化。最近的研究表明,脂肪组织分泌的细胞因子如瘦素和脂联素,通过与甲状腺激素协同调节食欲、肥胖和胰岛素敏感性来发挥其内分泌功能。甲状腺激素、胰岛素抵抗和脂肪因子之间的相互关系尚不清楚。
评估甲状腺功能减退患者的血清瘦素、脂联素和胰岛素抵抗,并与对照组进行比较,测量一个变量的平均值与其他变量之间的关系。
选取40例原发性甲状腺功能减退患者和40例年龄、性别匹配的对照者,均签署知情同意书参与研究。检测空腹血清促甲状腺激素(TSH)、瘦素、脂联素、血糖和胰岛素水平。根据空腹血糖和血清胰岛素水平评估胰岛素抵抗的稳态模型评估(HOMA-IR)。使用SPSS 17.0版进行统计分析。采用非配对t检验和回归分析进行比较并确定相关性,p<0.05被认为具有统计学意义。
甲状腺功能减退患者的血清TSH、瘦素、脂联素HOMA-IR显著高于对照组(分别为10.37±4.10、10.97±0.60、31.09±4.07、3.64±0.40,p<0.05)(对照组分别为2.41±2.09、10.37±0.12、33.32±1.44、2.36±0.35)。回归分析表明,瘦素显著依赖于脂联素(p=0.054),而不依赖于其他因素。
甲状腺功能减退介导的瘦素分泌增加和胰岛素抵抗增加所导致的氧化应激增加,可下调脂联素分泌及未来并发症。对甲状腺功能减退患者进行血清脂肪因子评估及失衡纠正可预防严重后果。