Hays J H, Silverman E, Potter B B, Shakir K M
Department of Medicine, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20889-4799.
J Endocrinol. 1994 Feb;140(2):309-12. doi: 10.1677/joe.0.1400309.
Although the action of gastric inhibitory polypeptide (GIP) on the beta cells of the pancreas is well documented, the effect of this hormone on insulin secretion in patients who are hypothyroid has not been studied. Hypothyroid patients demonstrate increased serum immunoreactive insulin levels in response to oral glucose when compared with euthyroid subjects. We postulated that a delayed and exaggerated response of GIP could account for the hyperinsulinaemic response. Nine thyroidectomized patients (aged 44.9 +/- 3.6 years) who were otherwise healthy but undergoing re-evaluation for recurrence of thyroid carcinoma, were given a 75 g oral glucose tolerance test (OGTT). These subjects were studied 6 weeks after thyroid hormone replacement had been stopped and while on hormone treatment. The serum glucose and plasma GIP responses to oral glucose were similar in the euthyroid and hypothyroid states. The serum insulin response as well as the areas under the curve for insulin following OGTT were significantly elevated (P < 0.01) during hypothyroidism. Solid-phase gastric emptying times studied in six patients who were euthyroid and hypothyroid were not different (35 +/- 12 versus 36 +/- 14 min respectively). None of the subjects had detectable levels of serum thyroglobulin, microsomal or parietal cell antibodies. In summary, we have confirmed a hyperinsulinaemic response to an OGTT and normal solid-phase gastric emptying rates in this form of hypothyroidism. We did not find significant differences in serum glucose or GIP responses and postulate this as evidence of resistance to the effects of endogenous insulin. The mechanism of alterations in carbohydrate tolerance in the hypothyroid state continue to remain unknown.
尽管胃抑制性多肽（GIP）对胰腺β细胞的作用已有充分记载，但该激素对甲状腺功能减退患者胰岛素分泌的影响尚未得到研究。与甲状腺功能正常的受试者相比，甲状腺功能减退患者口服葡萄糖后血清免疫反应性胰岛素水平升高。我们推测，GIP反应延迟和过度可能是导致高胰岛素血症反应的原因。9名甲状腺切除患者（年龄44.9±3.6岁），他们身体健康，但因甲状腺癌复发正在接受重新评估，接受了75g口服葡萄糖耐量试验（OGTT）。这些受试者在停止甲状腺激素替代治疗6周后以及接受激素治疗期间接受了研究。甲状腺功能正常和减退状态下，口服葡萄糖后血清葡萄糖和血浆GIP反应相似。甲状腺功能减退期间，血清胰岛素反应以及OGTT后胰岛素曲线下面积显著升高（P<0.01）。对6名甲状腺功能正常和减退的患者进行的固相胃排空时间研究结果无差异（分别为35±12分钟和36±14分钟）。所有受试者血清甲状腺球蛋白、微粒体或壁细胞抗体水平均未检测到。总之，我们证实了这种形式的甲状腺功能减退患者对OGTT有高胰岛素血症反应且固相胃排空率正常。我们未发现血清葡萄糖或GIP反应有显著差异，并推测这是对内源性胰岛素作用产生抵抗的证据。甲状腺功能减退状态下碳水化合物耐量改变的机制仍然未知。
