Longkumer Chubalemla, Nath Chandan Kr, Barman Bhupen, Ruram Alice Abraham, Visi Vizovonuo, Yasir M D, Sangma Merrycka Agitok
Department of Biochemistry, Neigrihms, Shillong-18, Meghalaya, India.
Department of Medicine, Neigrihms, Shillong-18, Meghalaya, India.
J Family Med Prim Care. 2020 Sep 30;9(9):4637-4640. doi: 10.4103/jfmpc.jfmpc_867_20. eCollection 2020 Sep.
There has been a lot of confusion in management of apparently healthy individuals whose post prandial plasma glucose levels were lower than fasting levels. It has been observed that many clinicians do send for repeat tests to rule out analytical error since there is common knowledge that post prandial glucose should be higher than fasting glucose level. Blood glucose level is regulated by a fully integrated mechanism with complex interplay of hormones and enzymes on metabolic pathways. Increase or decrease of thyroid hormones can break this equilibrium leading to alterations of carbohydrate metabolism. The objective for this study was to look for subclinical hypothyroidism (SCH) and insulin resistance (IR) in Idiopathic Post prandial glucose lowering and the correlation between thyroid stimulating hormone (TSH) with IR in them.
A cross-sectional study with subgroup analysis, 34 cases and 34 controls. Cases comprises of otherwise healthy individuals whose post prandial glucose is lower than fasting glucose and controls as those healthy individual whose post prandial glucose is higher than fasting. Thyroid hormones and insulin were measured in fasting serum samples. Homeostasis model assessment for IR was calculated as per formula.
Among the 34 cases with idiopathic post prandial glucose lowering, 76% ( = 26) had subclinical hypothyroidism and 61% ( = 21) had insulin resistance. A positive correlation (r = 0.55) was observed between Thyroid-Stimulating hormone (TSH) and Index of insulin resistance and homeostatic model assessment (HOMA-IR) and was statistically significant with < 0.1.
The study highlights the importance of evaluating glycoregulatory hormones like thyroid hormones and insulin in cases with idiopathic post prandial glucose lowering for early diagnosis and prevention of overt clinical diseases like Hypothyroidism and Diabetes Mellitus.
对于餐后血糖水平低于空腹血糖水平的健康个体，其管理存在诸多困惑。据观察，许多临床医生会要求进行重复检测以排除分析误差，因为大家都知道餐后血糖应高于空腹血糖水平。血糖水平由一个完全整合的机制调节，激素和酶在代谢途径中复杂地相互作用。甲状腺激素的增加或减少会打破这种平衡，导致碳水化合物代谢改变。本研究的目的是在特发性餐后血糖降低患者中寻找亚临床甲状腺功能减退（SCH）和胰岛素抵抗（IR），以及促甲状腺激素（TSH）与IR之间的相关性。
一项采用亚组分析的横断面研究，34例病例和34例对照。病例组为餐后血糖低于空腹血糖的健康个体，对照组为餐后血糖高于空腹血糖的健康个体。在空腹血清样本中测量甲状腺激素和胰岛素。根据公式计算IR的稳态模型评估值。
在34例特发性餐后血糖降低的病例中，76%（=26）有亚临床甲状腺功能减退，61%（=21）有胰岛素抵抗。促甲状腺激素（TSH）与胰岛素抵抗指数和稳态模型评估（HOMA-IR）之间存在正相关（r = 0.55），且具有统计学意义（P < 0.1）。
该研究强调了在特发性餐后血糖降低的病例中评估甲状腺激素和胰岛素等糖调节激素对于早期诊断和预防甲状腺功能减退和糖尿病等明显临床疾病的重要性。
