Although animal studies suggest that it is the uncarboxylated rather than carboxylated form of osteocalcin that affects glucose homeostasis, the human data are scant and equivocal.
The etiology of cardiovascular disease (CVD) starts in childhood. This may be manifested as unhealthy levels of insulin, blood pressure, lipids, and heart rate (HR). Physical activity (PA) interventions have been successful in ameliorating CVD risk factors in overweight children and adolescents. PURPOSE: To determine the effects of a 10-mo PA intervention on CVD risk factors in 8–12 y old black girls not selected for adiposity levels (range for percent body fat (%BF): 10 to 56%). METHODS: Subjects were randomized to the intervention (n=118) or control (n=82) group. The intervention included 80 min of PA every day after school. CVD risk factors included resting HR and blood pressure obtained from Dinamap, and fasting levels of insulin, glucose, cholesterol, lipoproteins, apolipoproteins, triglycerides, C-reactive protein and fibrinogen. %BF was obtained from dual-energy x-ray absorptiometry. Height and weight were measured to calculate body mass index (BMI) from which the BMI percentile for age and sex for each subject was obtained. The change in each group for the CVD risk factors was compared using analysis of covariance; covariates included age, baseline value of the dependent variable, and either BMI percentile or change in %BF. Results are reported as adjusted relative change (95% confidence interval). RESUITS: Beneficial effects of the PA were seen in the intervention group compared to the control group for resting HR (−2.7 (−3.8, −1.66) bpm, p=0.01), low density lipoprotein cholesterol (−0.20 (−0.30, −1.91) mmol/L, p=0.04), and a trend for C-reactive protein (−245.8 (−391.0, 100.7) ng/mL, p=0.09). BMI percentile and change in %BF were not significantly associated with changes in the CVD risk factors. CONCLUSIONS: This study showed that regular PA can have beneficial effects on some CVD risk factors in children of all adiposity levels. This is evidence that PA interventions should not be aimed only at overweight children, but that all children may benefit from such programs. Supported by NIH HL 64972.
Vitamin D insufficiency/deficiency is commonly observed in black youth.The aim was to determine 25-hydroxyvitamin D [25(OH)D] in response to 2000 IU vitamin D supplementation over time; to evaluate the relation between 25(OH)D concentrations and total body fat mass by dual-energy x-ray absorptiometry; and to determine whether vitamin D supplementation improves arterial stiffness measured by pulse wave velocity (PWV).We conducted a randomized, blinded, controlled clinical trial.Forty-nine normotensive black boys and girls, aged 16.3 ± 1.4 yr, were randomly assigned to either the control group (400 IU/d; n = 24) or the experimental group (2000 IU/d; n = 25).Plasma 25(OH)D values at baseline and at 4, 8, and 16 wk were 34.0 ± 10.6, 44.9 ± 9.4, 51.2 ± 11.1, and 59.8 ± 18.2 nmol/liter, respectively, for the control group; and 33.1 ± 8.7, 55.0 ± 11.8, 70.9 ± 22.0, and 85.7 ± 30.1 nmol/liter, respectively, for the experimental group. The experimental group vs. the control group reached significantly higher 25(OH)D concentrations at 8 and 16 wk, respectively. Partial correlation analyses indicated that total body fat mass at baseline was significantly and inversely associated with 25(OH)D concentrations in response to the 2000-IU supplement across time. Furthermore, carotid-femoral PWV increased from baseline (5.38 ± 0.53 m/sec) to posttest (5.71 ± 0.75 m/sec) in the control group (P = 0.016), whereas in the experimental group carotid-femoral PWV decreased from baseline (5.41 ± 0.73 m/sec) to posttest (5.33 ± 0.79 m/sec) (P = 0.031).Daily 2000 IU vitamin D supplementation may be effective in optimizing vitamin D status and counteracting the progression of aortic stiffness in black youth. Plasma 25(OH)D concentrations in response to the 2000 IU/d supplementation are negatively modulated by adiposity.
The childhood obesity surge has led to a larger population of children with dyslipidemia. Without intervention, dyslipidemia is likely to become atherosclerotic cardiovascular disease in adulthood. Menaquinones, also known as vitamin K 2, have been recently focused as a pivotal nutrient in improvement in lipid related parameters, possibly via increased carboxylation of matrix Gla‐protein (MGP). Therefore, this study investigated the dose‐response effect of menaquinone‐7 (MK‐7) supplementation on lipid profile and the inactive form of MGP (dephospho‐uncarboxylated MGP, dp‐ucMGP) in obese African‐American (AA) children. Associations between the changes in dp‐ucMGP and the changes in lipid related parameters were also determined. Fifteen obese AA children (mean age, 12.3 ± 2.9 years; mean BMI percentile, 98.8 ± 1.0; 60% female) were randomly allocated to either the control group receiving placebo or the low‐dose (45‐μg/d) or high‐dose group (90‐μg/d) receiving MK‐7 supplementation for 8 weeks. At baseline and posttest, fasting blood samples were collected for assessment of serum levels of triglycerides, total cholesterol, HDL‐cholesterol, non‐HDL‐cholesterol and LDL‐cholesterol, and plasma levels of dp‐ucMGP. After 8 weeks, dp‐ucMGP decreased significantly and dose‐dependently in the 45‐μg and 90‐μg MK‐7 supplementation groups by 8% and 22%, respectively ( P =0.02). A dose‐response benefit of MK‐7 supplementation was also observed for triglycerides, total cholesterol, non‐HDL‐cholesterol, and LDL‐cholesterol as indicated by significant downward trends (all P < 0.05). There was no dose‐response effect of MK‐7 on HDL‐cholesterol. Pearson's bivariate analyses revealed that changes in triglycerides ( r = 0.69) and non‐HDL cholesterol ( r = 0.65) were associated with changes in dp‐ucMGP (both P < 0.04). After 8‐weeks, MK‐7 supplementation demonstrated dose‐response benefits on lipid profile in obese children. Our study provides the rationale that larger intervention trials are needed to determine whether vitamin K 2 supplementation slows atherosclerosis development by increasing MGP carboxylation. Support or Funding Information This work was funded by Georgia Regents University's Intramural Grants Program.
