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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/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.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. [ABSTRACT FROM AUTHOR]

Obesity is frequently characterized by a reduced vitamin D bioavailability, as well as insulin-resistance and a chronic inflammatory response. We tested the hypothesis of an independent relationship between serum concentrations of 25-hydroxyvitamin D (25[OH]D) and several circulating inflammatory markers in a cohort of severely obese individuals. Cross-sectional study was carried out among obese patients undergoing a clinical evaluation before bariatric surgery in our University Hospital. Serum 25(OH)D, fasting and post load glucose and insulin, high-sensitive C-reactive protein (hs CRP), fibrinogen, interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), leptin, adiponectin and lipid profile were collected. Insulin-resistance was assessed by insulin sensitivity index (ISI). Total body fat (FAT kg), total percent body fat (FAT%) and truncal fat mass (TrFAT) were assessed with dual-energy X-ray absorptiometry. A total of 147 obese subjects (89 women, 37.8 ± 7.1 years) with mean body mass index (BMI) of 43.6 ± 4.3 kg/m were enrolled. Patients in the lowest tertile of 25(OH)D were significantly more obese with a higher amount of TrFAT, more insulin-resistant, and had higher levels of fasting and post-challenge glucose ( p < 0.05 for all). In a multivariate regression analysis, serum 25(OH)D was inversely related to significant levels of hs CRP, IL-6 and TNF-α after accounting for age, gender, season of recruitment, BMI, FAT kg and TrFAT ( p < 0.01 for all). In extremely obese subjects, 25(OH)D serum concentrations are inversely associated with several biomarkers of systemic inflammation, regardless of the total quantity of fat mass. [ABSTRACT FROM AUTHOR]