Parathyroid hormone in surgery-induced weight loss: no glucometabolic effects but potential adaptive response to skeletal loading.

Abstract

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 explorethe 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. We included 42 subjects (27 women, aged 40 ± 5 years, BMI 48.5 ± 7.3 kg/m2) 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. 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). 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.