1.
Vitamin D kinetics in nonpregnant and pregnant women after a single oral dose of trideuterated vitamin D3.
Best, CM, Sherwood, R, Novotny, JA, Zhang, S, Pressman, EK, O'Brien, KO
The Journal of steroid biochemistry and molecular biology. 2022;:106034
-
-
Free full text
-
Abstract
The plasma pool of the hormone 1,25-dihydroxyvitamin D (1,25(OH)2D) is increased throughout most of human pregnancy. Mechanisms behind this adaptation are unclear, in part due to limited data on vitamin D kinetics during pregnancy. Stable isotopes make it possible to study vitamin D kinetics in vulnerable study populations like pregnant women. We conducted a pilot study of vitamin D kinetics in nonpregnant and pregnant women. We evaluated a clinical protocol and developed analytical methods to assess the serum appearance and disappearance of trideuterated vitamin D3 (d3-vitamin D3) and trideuterated 25-hydroxyvitamin D3 (d3-25(OH)D3) after a single oral dose of 25 μg of [6,19,19-2H]-vitamin D3 (d3-vitamin D3). Blood was collected at baseline and 2, 4, 6, 24, 168, 264, and 456 hours post-dosing. We then described the serum kinetic profiles of d3-vitamin D3 and d3-25(OH)D3 in nonpregnant and pregnant women. Serum kinetic profiles of d3-vitamin D3 and d3-25(OH)D3 followed a time course in line with previous pharmacokinetic studies. There was marked variability between participants in the area under the concentration-time curve (AUC) of d3-25(OH)D3 over the 20-day study period. This AUC of d3-25(OH)D3 was positively correlated with the serum vitamin D binding protein (DBP) concentration, which was higher in pregnant compared with nonpregnant women. The mean serum half-life of 25(OH)D3 was longer but not significantly different in pregnant women (18.8 days) compared with nonpregnant women (13.6 days). Our pilot study demonstrated that a single oral dose of 25 μg of d3-vitamin D3 can be used to study vitamin D kinetics. Serum DBP concentration is an important predictor of vitamin D kinetics, and more research is needed to fully understand the significance of elevated DBP concentration during pregnancy.
2.
Natural sunlight plus vitamin D supplementation ameliorate delayed early motor development in newborn infants from maternal perinatal depression.
Zhang, H, Liu, S, Si, Y, Zhang, S, Tian, Y, Liu, Y, Li, H, Zhu, Z
Journal of affective disorders. 2019;:241-249
Abstract
BACKGROUND Increased cortisol has been shown to be negatively correlated with infant motor development. Sunlight help decrease the level of cortisol. Vitamin D is associated with infant motor development. The present study aimed to determine whether natural sunlight exposure plus vitamin D supplements could ameliorate delayed early motor development in little infants from maternal perinatal depression. METHODS The term pregnant women waiting for delivery from the department of gynecology and obstetrics were assessed depressive symptoms by Hamilton Rating Scale for Depression (HAMD). 120 normal and 229 depressed subjects were recruited. During 2 days postpartum, infant motor development were assessed by Neonatal Behavioral Assessment Scale (NBAS). Infants of 2-day-old in maternal depression group were divided into four groups: control group, conventional vitamin D supplements (400IU/d) group, high dose of vitamin D supplements group (1000IU/d), sunlight plus conventional vitamin D supplement group (400IU/d). Serum and hair cortisol (HairF) in mothers and infants were measured. RESULTS The infants of perinatal depressed mothers displayed early motor developmental delay accompanied by increased cortisol. Sunlight plus conventional vitamin D supplement (400IU/d) were better than exclusive vitamin D supplements for the amelioration delayed early motor development in infants (p < 0.05). The infants exposure to sunlight 7-14 h/week plus conventional vitamin D supplement reached the best scores of motor development and the lowest HairF (p < 0.05). LIMITATIONS We should have measured the serum 25OH-vitamin D concentrations. CONCLUSIONS Sunlight plus vitamin D supplements could ameliorate delayed early motor development in little infants by decreasing cortisol from perinatal depression.
3.
Decreased conversion of 25-hydroxyvitamin D3 to 24,25-dihydroxyvitamin D3 following cholecalciferol therapy in patients with CKD.
Stubbs, JR, Zhang, S, Friedman, PA, Nolin, TD
Clinical journal of the American Society of Nephrology : CJASN. 2014;(11):1965-73
-
-
Free full text
-
Abstract
BACKGROUND AND OBJECTIVES Elevated concentrations of fibroblast growth factor 23 (FGF23) are postulated to promote 25-hydroxyvitamin D (25[OH]D) insufficiency in CKD by stimulating 24-hydroxylation of this metabolite, leading to its subsequent degradation; however, prospective human studies testing this relationship are lacking. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS An open-label prospective study was conducted from October 2010 through July 2012 to compare the effect of 8 weeks of oral cholecalciferol therapy (50,000 IU twice weekly) on the production of 24,25(OH)2D3 in vitamin D-insufficient patients with CKD (n=15) and controls with normal kidney function (n=15). Vitamin D metabolites were comprehensively profiled at baseline and after treatment, along with FGF23 and other mineral metabolism parameters. RESULTS Vitamin D3 and 25(OH)D3 concentrations increased equivalently in the CKD and control groups following cholecalciferol treatment (median D3 change, 8.6 ng/ml [interquartile range, 3.9-25.6 ng/ml] for controls versus 12.6 ng/ml [6.9-41.2 ng/ml] for CKD [P=0.15]; 25(OH)D3 change, 39.2 ng/ml [30.9-47.2 ng/ml] for controls versus 39.9 ng/ml [31.5-44.1 ng/ml] for CKD [P=0.58]). Likewise, the absolute increase in 1α,25(OH)2D3 was similar between CKD participants and controls (change, 111.2 pg/ml [64.3-141.6 pg/ml] for controls versus 101.1 pg/ml [74.2-123.1 pg/ml] for CKD; P=0.38). Baseline and post-treatment 24,25(OH)2D3 concentrations were lower in the CKD group; moreover, the absolute increase in 24,25(OH)2D3 after therapy was markedly smaller in patients with CKD (change, 2.8 ng/ml [2.3-3.5 ng/ml] for controls versus 1.2 ng/ml [0.6-1.9 ng/ml] for patients with CKD; P<0.001). Furthermore, higher baseline FGF23 concentrations were associated with smaller increments in 24,25(OH)2D3 for individuals with CKD; this association was negated after adjustment for eGFR by multivariate analysis. CONCLUSIONS Patients with CKD exhibit an altered ability to increase serum 24,25(OH)2D3 after cholecalciferol therapy, suggesting decreased 24-hydroxylase activity in CKD. The observed relationship between baseline FGF23 and increments in 24,25(OH)2D3 further refutes the idea that FGF23 directly contributes to 25(OH)D insufficiency in CKD through stimulation of 24-hydroxylase activity.