Vitamin K is found in the diet in two biologically active forms, phylloquinone (vitamin K1) and menaquinone (vitamin K2). Phylloquinone is found in green leafy plants and some oils and is the predominate form in the human diet, whereas the menaquinones occur mainly in cheese, meat and eggs. Nutritionally vitamin K is important because it is a cofactor in the γ-glutamyl carboxylation of γ-carboxyglutamate residues present in vitamin K dependent proteins (VKDP), and is essential for their function. The VKDP have a wide ranging biological activity and can include osteocalcin, matrix γ-carboxyglutamate protein and Gas6, which are involved in bone turnover, inhibition of vascular calcification, and the inhibition of apoptosis and proliferation, respectively. Recent evidence suggests that vitamin K may play a role in metabolic syndrome through the activity of osteocalcin, which in a hormonal role can have profound effects on energy metabolism and fat deposition.
Animal models that produce a deficiency of osteocalcin result in phenotype in mice that resembles the metabolic abnormalities seen in metabolic syndrome. Increasing the osteocalcin concentrations above normal results in reversal of the condition through increase insulin sensitivity. Osteocalcin appears to stimulate the β-cells of the pancreas to produce insulin, and also promotes the growth of new β-cells. In addition, osteocalcin stimulates the release of adiponectin, a cytokine released from adipose tissue that increases insulin sensitivity. Long term administration of osteocalcin in animal models reduces the deleterious effect of a high fat diet and experimentally induced hyperphagia on body mass gains and glucose metabolism abnormalities. Vitamin K deficiency results in uncarboxylated γ-carboxyglutamate residues on VKDP and so the activity of those proteins is diminished or missing completely. Therefore the relationship between vitamin K intake and metabolic syndrome is of interest to nutritional researchers.
One study published in the Journal of the American College of Nutrition1 investigated the relationship between phylloquinone intake and metabolic syndrome in a cross sectional study of 5800 adults aged 20 to 45 years. The data was collected from the National Health and Nutritional Examination Survey (NHANES) between 1999 and 2004. Central obesity, dyslipidaemia (high triglycerides and low high-density lipoprotein [HDL] cholesterol), elevated blood pressure and glucose intolerance, the 5 components that make up the metabolic syndrome, were most prevalent in those with the lowest intakes of phylloquinone. Progressively increasing phylloquinone intake was associated with a progressive decrease in the prevalence of elevated blood pressure and low levels of HDL. Increased intakes of phylloquinone were also associated with decreased levels of C-reactive protein, a marker for systemic inflammation that can be elevated in subjects with central adiposity and metabolic syndrome.
In general, those individuals in the highest quartile for phylloquinone intake had a reduced risk for developing low HDL levels, hypertriglyceridaemia and hyperglycaemia following adjustment for non-dietary confounding variables. However, only the association between phylloquinone intake and hyperglycaemia remained after adjustment for other dietary confounding variables. Therefore, it is likely that phylloquinone intake does have an association with some aspects of the metabolic syndrome, but a high intake of phylloquinone may favourable affect the risk of metabolic syndrome predominately as part of a healthy diet and lifestyle. Previous studies have shown that the Mediterranean diet, a diet high in green leafy plants rich in vitamin K, is beneficial in the treatment of metabolic syndrome. Because of the complexity of the metabolic syndrome, in combination with the decades it takes to manifest, it would be unexpected for deficiency of a single dietary component to be wholly responsible for its development.
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