Obesity is often associated with vitamin D deficiency and secondary hyperparathyroidism. Vitamin D supplementation typically leads to the reductions in serum parathyroid hormone (PTH) levels, as shown in normal weight individuals. Meanwhile, the dose of vitamin D supplementation for the suppression of PTH may differ in overweight and obese adults. We conducted a systematic review and meta-analysis of randomized controlled trials to determine the dose of vitamin D supplementation required to suppress PTH levels in overweight/obese individuals. We identified 18 studies that examined overweight or obese healthy adults who were supplemented with varying doses of vitamin D3. The primary outcomes examined were changes in PTH and serum 25-hydroxyvitamin D (25OHD) levels from baseline to post-treatment. The results of the meta-analysis showed that there was a significant treatment effect of vitamin D supplementation on PTH, total standardized mean difference (SMD) (random effects) = −0.38 (95% CI = −0.56 to −0.20), t = −4.08, p < 0.001. A significant treatment effect of vitamin D supplementation was also found on 25OHD, total SMD (random effects) = 2.27 (95% CI = 1.48 to 3.06) t = 5.62, p < 0.001. Data from available clinical trials that supplemented adults with D3 ranging from 400 IU to 5714 IU, showed that 1000 IU of vitamin D supplementation best suppressed serum PTH levels, total SMD = −0.58, while vitamin D supplementation with 4000 IU showed the greatest increase in serum 25OH levels. Vitamin D and calcium supplementation of 700 IU and 500 mg, respectively, also showed a significant treatment effect on the suppression of PTH with a total SMD = −5.30 (95% CI = −9.72 to −0.88). In conclusion, the meta analysis of available clinical trials indicates that 1000 IU vitamin D supplementation can suppress serum PTH levels, while 4000 IU of vitamin D was associated with the largest increase in serum 25OHD levels in the overweight and obese population.

These findings suggest that bone-regulating hormones and nutrients, especially serum PTH, osteocalcin concentrations, and dietary Mg intakes, can help to characterize the MHO phenotype.

The term Metabolically healthy obese (MHO) phenotype has been used to describe those who present with a benign metabolic profile despite excess adiposity. These individuals are obese but are either completely free of metabolic abnormalities or have less than three components of metabolic syndrome. Previous studies suggest that bone regulating hormones and nutrients, such as parathyroid hormone (PTH), 25‐hydroxyvitamin D (25OHD), estrogen, osteocalcin, vitamin D, calcium and magnesium (Mg) influence overall energy metabolism. In this study, we aim to determine whether bone regulating hormones and nutrients can help characterize the MHO phenotype. We hypothesize that adequate Mg status, higher serum 25OHD and lower serum PTH concentrations are variable that could be included in the characterization of the MHP phenotype. A total of 27 overweight or obese adults (BMI 25–40 kg/m2) were recruited. Measurements were obtained for ionized Mg, serum 25OHD, serum PTH, body fat percentage, trunk fat percentage, total fat mass, blood pressure, glycemic indices, lipid profile, and pro‐inflammatory cytokines in order to determine the metabolic factors differentiating MHO vs metabolically unhealthy obese (MUO) in this sample. Based on the presence of metabolic abnormalities, participants were classified as MHO (n=13) or MUO (n=14). Results showed no significant difference in mean age between the MHO group and MUO group (Mean age : 32.6 ± 9.2 yr). As expected, serum insulin concentrations and diastolic BP were lower in the MHO group compared to the MUO group (p < 0.04). In addition, triglyceride and c‐reactive protein concentrations did not differ between groups. Dietary Mg intake tended to be higher in the MHO group (270.4 ± 181.7 mg/day) than the MUO group (195.4 ± 88.9 mg/day). Ionized Mg concentration was significantly higher (p < 0.04) in the MHO group than in the MUO group. Serum 25OHD concentrations did not differ between groups, while serum PTH concentrations were significantly higher (p < 0.02) in the MUO group (61.8 ± 25.9 pg/mL) than the MHO group (40.2 ± 11.5 pg/mL). Serum osteocalcin and serum c‐telopeptide collagen concentrations also tended to be higher in the MHO compared to the MUO group. In summary the MHO phenotype had a better magnesium status, lower serum PTH levels and higher serum levels of bone turnover markers, some of which have shown to regulate energy metabolism. Early recognition of the alterations in these bone regulating hormones and nutrients can be a potential target for intervention or prevention of metabolic abnormalities in the obese population.Support or Funding InformationAmerican Heart Association‐ Scientist Development Grant‐ 16SDG27050002 to Deeptha Sukumar