Department of Systems Medicine, Laboratory of Molecular Medicine, University of Rome Tor Vergata, Rome, Italy.
Obesity Center and Internal Medicine Unit, University Hospital Policlinico Tor Vergata, Rome, Italy.
Endocrine. 2018 Feb;59(2):288-295. doi: 10.1007/s12020-017-1477-0. Epub 2017 Nov 22.
PURPOSE: Increased parathyroid hormone (PTH) is commonly associated with obesity, and its role in the pathogenesis of obesity-related glucometabolic abnormalities is uncertain. We aimed to explore the relationships of PTH with glucose/insulin homeostasis parameters before and after bariatric surgery-induced weight loss, and whether they depend or not on 25-hydroxyvitamin D (25OHD) status. METHODS: We included 42 subjects (27 women, aged 40 ± 5 years, BMI 48.5 ± 7.3 kg/m) without diabetes, chronic kidney disease, or hyperparathyroidism undergoing sleeve gastrectomy. The following parameters were evaluated before and 6 months after surgery: circulating levels of PTH, calcium, phosphorus, 25OHD, leptin, insulin growth factor (IGF)-1; 75-g oral glucose tolerance test to derive measures of insulin sensitivity (ISI) and secretion (Stumvoll index); dual-energy X-ray absorptiometry to assess fat distribution and bone mineral density. RESULTS: Weight loss was accompanied by significant reduction of PTH levels (77.9 ± 19.1 vs. 60.5 ± 13.4 pg/ml; p = 0.005), without concomitant modification of 25OHD status. Both baseline PTH and its postoperative percent change resulted associated, with baseline fat mass (β = 0.615, p = 0.003) and its concurrent postoperative reduction (r = 0.419; p = 0.006), but neither with glucose homeostasis parameters nor their respective variations after weight loss. Interestingly, leptin reduction after weight loss was independently related to PTH change (β = 0.396, p = 0.015) and IGF-1 levels (β = 0.176, p = 0.059). CONCLUSIONS: Circulating PTH decreases with fat mass reduction independent of 25OHD status, but it is not associated with improvement of insulin resistance and related metabolic parameters. Leptin and PTH may mediate the cross-talk between adipose tissue and parathyroid glands, which possibly contributes to bone adaptation to excess body weight.
目的:甲状旁腺激素(PTH)升高通常与肥胖有关,但其在肥胖相关糖代谢异常发病机制中的作用尚不确定。本研究旨在探讨减重手术后 PTH 与葡萄糖/胰岛素稳态参数的关系,并分析其是否依赖于 25-羟维生素 D(25OHD)状态。
方法:本研究纳入 42 例(27 名女性,年龄 40±5 岁,BMI 48.5±7.3kg/m2)无糖尿病、慢性肾脏病或甲状旁腺功能亢进症的患者,接受袖状胃切除术。分别在术前和术后 6 个月检测以下参数:循环 PTH、钙、磷、25OHD、瘦素、胰岛素生长因子(IGF)-1 水平;口服 75g 葡萄糖耐量试验(OGTT)以评估胰岛素敏感性(ISI)和分泌(Stumvoll 指数);双能 X 线吸收法评估体脂分布和骨密度。
结果:体重减轻伴随着 PTH 水平显著降低(77.9±19.1 vs. 60.5±13.4pg/ml;p=0.005),而 25OHD 状态无明显变化。基线 PTH 及其术后变化百分比均与基线脂肪量(β=0.615,p=0.003)及其术后同期减少(r=0.419;p=0.006)相关,但与葡萄糖稳态参数及其术后变化均无关。有趣的是,减重后瘦素的减少与 PTH 的变化(β=0.396,p=0.015)和 IGF-1 水平(β=0.176,p=0.059)独立相关。
结论:PTH 随着脂肪量的减少而降低,独立于 25OHD 状态,但与胰岛素抵抗和相关代谢参数的改善无关。瘦素和 PTH 可能介导脂肪组织和甲状旁腺之间的相互作用,这可能有助于骨适应超重。
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