Tosi F, Moghetti P, Castello R, Negri C, Bonora E, Muggeo M
Division of Endocrinology and Metabolic Diseases, University of Verona, Ospedale Maggiore, Italy.
Metabolism. 1996 Aug;45(8):1029-33. doi: 10.1016/s0026-0495(96)90275-9.
The mechanisms underlying deterioration of glucose tolerance associated with hyperthyroidism are not completely understood. Increases in glucagon and growth hormone (GH) secretion have been previously found in hyperthyroid subjects, and could play a crucial role in this phenomenon. However, studies have not yet established the time sequence of changes in plasma glucose on the one hand and glucagon and GH on the other. To assess the early effects of thyroid hormone excess on glucose tolerance and plasma concentrations of the main glucoregulatory hormones, 12 nondiabetic euthyroid subjects underwent an oral glucose tolerance test (OGTT) before and after triiodothyronine ([T3] 120 micrograms/d) was administered for 10 days. Plasma levels of glucose, insulin, glucagon, and GH were determined at fasting and after the glucose load. T3 administration caused a marked increase in serum T3 (8.8 +/- 0.6 v 2.0 +/- 0.1 nmol/L), with clinical and biochemical signs of thyrotoxicosis. During the treatment, plasma glucose significantly increased both at fasting and after the glucose load (basal, 5.3 +/- 0.1 v 4.9 +/- 0.2 mmol/L, P < .05; area under the curve [AUC] for OGTT, 7.7 +/- 0.3 v 6.7 +/- 0.4 mmol/L min, P < .01) without any change in plasma insulin levels. After T3 administration, plasma glucagon levels were lower than at baseline (basal, 92 +/- 7 v 148 +/- 35 ng/L; AUC, 74 +/- 6 v 98 +/- 16 ng/L.min, P < .05), showing an appropriate reduction by the increased glucose levels. Conversely, plasma GH showed impaired suppression by hyperglycemia (AUC, 1.2 +/- 0.3 v 0.7 +/- 0.2 microgram/L.min, P < .05). In conclusion, thyroid hormone excess rapidly impairs glucose tolerance. Altered secretion of GH is an early event in thyrotoxicosis accompanying the onset of hyperglycemia, whereas plasma glucagon is appropriately suppressed by the increased plasma glucose levels. Thus, GH but not glucagon may contribute to the early hyperglycemic effect of thyrotoxicosis.
甲状腺功能亢进症相关糖耐量恶化的潜在机制尚未完全明确。先前在甲状腺功能亢进的受试者中发现胰高血糖素和生长激素（GH）分泌增加，这可能在该现象中起关键作用。然而，研究尚未确定一方面血浆葡萄糖与另一方面胰高血糖素和GH变化的时间顺序。为了评估甲状腺激素过量对糖耐量和主要血糖调节激素血浆浓度的早期影响，12名非糖尿病甲状腺功能正常的受试者在给予三碘甲状腺原氨酸（[T3]120微克/天）10天前后进行了口服葡萄糖耐量试验（OGTT）。在空腹和葡萄糖负荷后测定血浆葡萄糖、胰岛素、胰高血糖素和GH水平。给予T3导致血清T3显著升高（8.8±0.6对2.0±0.1纳摩尔/升），伴有甲状腺毒症的临床和生化体征。在治疗期间，空腹和葡萄糖负荷后血浆葡萄糖均显著升高（基础值，5.3±0.1对4.9±0.2毫摩尔/升，P<.05；OGTT曲线下面积[AUC]，7.7±0.3对6.7±0.4毫摩尔/升·分钟，P<.01），而血浆胰岛素水平无任何变化。给予T3后，血浆胰高血糖素水平低于基线（基础值，92±7对148±35纳克/升；AUC，74±6对98±16纳克/升·分钟，P<.05），表明随着血糖水平升高出现了适当降低。相反，血浆GH对高血糖的抑制作用受损（AUC，1.2±0.3对0.7±0.2微克/升·分钟，P<.05）。总之，甲状腺激素过量会迅速损害糖耐量。GH分泌改变是甲状腺毒症伴随高血糖发作的早期事件，而血浆胰高血糖素则被升高的血浆葡萄糖水平适当抑制。因此，可能是GH而非胰高血糖素促成了甲状腺毒症的早期高血糖效应。
