Animal studies have found that vitamin K-dependent proteins matrix Gla protein and osteocalcin beneficially influence lipid and glucose metabolism, respectively. However, this concept has not been tested in humans at risk for dyslipidemia and diabetes risk. Vitamin K supplementation presents an opportunity to test the hypothesized link between the vitamin K-dependent proteins and markers of lipid and glucose metabolism. The investigators will conduct an 8-week vitamin K intervention (to manipulate carboxylation of matrix Gla protein and osteocalcin) and determine its effects on markers of dyslipidemia and diabetes risk. Sixty obese children will be randomly allocated to either the control group receiving placebo or the low-dose (45 mcg/d) or high-dose group (90 mcg/d) receiving vitamin K (menaquinone-7).
Study Type
INTERVENTIONAL
Allocation
RANDOMIZED
Purpose
PREVENTION
Masking
QUADRUPLE
Enrollment
30
two placebo softgel capsules per day (for 8 weeks) containing no vitamin K2 (menaquinone-7)
one 45-mcg vitamin K2 (menaquinone-7) softgel capsule per day and one placebo softgel per day (containing no menaquinone-7) for 8 weeks
two 45-mcg vitamin K2 (menaquinone-7) softgel capsules per day for 8 weeks
Medical College of Georgia; Augusta University
Augusta, Georgia, United States
Change in serum lipid concentrations
To determine if the vitamin K-induced change in matrix Gla protein carboxylation improves fasting lipid panel (triglycerides, total cholesterol, HDL-cholesterol, and LDL-cholesterol) in a dose-dependent manner.
Time frame: 8 weeks
Change in insulin sensitivity
To determine if the vitamin K-induced change in osteocalcin carboxylation effects insulin sensitivity in a dose-dependent manner. Insulin sensitivity will be calculated from plasma insulin and glucose concentrations measured during a two-hour oral glucose tolerance test by using the oral glucose minimal model.
Time frame: 8 weeks
Change in beta-cell function
To determine if the vitamin K-induced change in osteocalcin carboxylation effects beta-cell function in a dose-dependent manner. Beta-cell function, as assessed by dynamic beta-cell responsitivity, will be calculated from plasma glucose and C-peptide concentrations measured during a two-hour oral glucose tolerance test by using the oral C-peptide minimal model.
Time frame: 8-weeks
Change in coagulation
Coagulation-related parameters (i.e., prothrombin time and activated partial thromboplastin time) will be assessed at baseline and 8 weeks to assess clotting function.
Time frame: 8 weeks
Change in arterial stiffness (pulse wave velocity)
Arterial stiffness, as measured by pulse wave velocity (PWV), will be assessed at baseline and 8 weeks to explore whether change in arterial stiffness is influenced by vitamin K2 supplementation.
Time frame: 8 weeks
Change in endothelial function (flow-mediated dilation)
Endothelial function, as measured by flow-mediated dilation (FMD), will be assessed at baseline and 8 weeks to explore whether change in endothelial function is influenced by vitamin K2 supplementation.
Time frame: 8 weeks
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