Division of Endocrinology and Metabolism, First Department of Internal Medicine, AHEPA Hospital, Medical School, Aristotle University of Thessaloniki, Thessaloniki, Greece.
Laboratories "Analysi Iatriki S.A.", Thessaloniki, Greece.
J Surg Res. 2020 Jan;245:22-30. doi: 10.1016/j.jss.2019.07.019. Epub 2019 Aug 7.
Although primary hyperparathyroidism has been associated with insulin resistance, potential optimal effects of parathyroidectomy (PTX) on glucose homeostasis remain controversial. Accordingly, the impact of PTX on glucose-stimulated incretin (glucagon-like peptide 1 [GLP-1] and gastric inhibitory peptide) secretion has not been evaluated. The aim of this pilot study was to compare glucose-stimulated incretin secretion (GSIS) in patients with asymptomatic primary hyperparathyroidism with normal glucose homeostasis, before and after PTX.
Fourteen patients were included in the study. Fasting calcium, parathyroid hormone, glucose, insulin, GLP-1, and gastric inhibitory peptide were measured pre- and post-operatively. Homeostasis Model Assessment 2, QUICKI, and Matsuda indexes were used as markers of insulin sensitivity and resistance before and after PTX. Preoperatively, a 75 g oral glucose tolerance test (OGTT) was performed to evaluate the response of glucose, insulin, and GSIS. OGTT measurements were repeated 6 ± 2 wk post-PTX.
Patients had a mean age of 52.93 ± 9.96 y, and female-to-male ratio was 12:2. Pre- and post-operatively, a positive correlation between parathyroid hormone and Homeostasis Model Assessment 2 for β-cell function was evident (r = 0.74, P = 0.002 and r = 0.55, P = 0.04, respectively). After PTX, a significant increase in GSIS for GLP-1 during OGTT was observed (in 60 min: 63.06 ± 44.78 versus 102.64 ± 40.19 pg/mL, P = 0.02; and in 120 min: 71.20 ± 35.90 versus 102.49 ± 40.02 pg/mL, P = 0.03).
The increase of GLP-1 response following oral glucose load after PTX may reflect an initial recovery phase of glucose homeostasis. Long-term studies are required to elucidate the physiological interplay between the normalization of calciotropic axis and the rising GLP-1 concentrations post-PTX.
尽管原发性甲状旁腺功能亢进与胰岛素抵抗有关，但甲状旁腺切除术（PTX）对葡萄糖稳态的潜在最佳影响仍存在争议。因此，尚未评估 PTX 对葡萄糖刺激肠降血糖素（胰高血糖素样肽 1 [GLP-1] 和胃抑制肽）分泌的影响。本初步研究的目的是比较无症状原发性甲状旁腺功能亢进且葡萄糖稳态正常的患者在 PTX 前后的葡萄糖刺激肠降血糖素分泌（GSIS）。
本研究纳入了 14 名患者。在术前和术后测量空腹钙、甲状旁腺激素、血糖、胰岛素、GLP-1 和胃抑制肽。在 PTX 前后使用稳态模型评估 2 型、QUICKI 和 Matsuda 指数作为胰岛素敏感性和抵抗的标志物。术前进行 75g 口服葡萄糖耐量试验（OGTT）以评估葡萄糖、胰岛素和 GSIS 的反应。OGTT 测量在 PTX 后 6±2 周重复进行。
患者的平均年龄为 52.93±9.96 岁，男女比例为 12:2。在术前和术后，甲状旁腺激素与稳态模型评估 2 型β细胞功能之间存在正相关（r=0.74，P=0.002 和 r=0.55，P=0.04）。PTX 后，OGTT 期间 GLP-1 的 GSIS 显著增加（60 分钟：63.06±44.78 与 102.64±40.19 pg/mL，P=0.02；120 分钟：71.20±35.90 与 102.49±40.02 pg/mL，P=0.03）。
PTX 后口服葡萄糖负荷后 GLP-1 反应增加可能反映了葡萄糖稳态的初始恢复阶段。需要进行长期研究以阐明钙调节轴正常化与 PTX 后 GLP-1 浓度升高之间的生理相互作用。
