The initial observations linking vitamin D to type 2 diabetes in humans came from studies showing that both healthy and diabetic subjects had a seasonal variation of glycemic control. Currently, there is evidence supporting that vitamin D status is important to regulate some pathways related to type 2 diabetes development. Since the activation of inflammatory pathways interferes with normal metabolism and disrupts proper insulin signaling, it is hypothesized that vitamin D could influence glucose homeostasis by modulating inflammatory response. Human studies investigating the impact of vitamin D supplementation on inflammatory biomarkers of subjects with or at high risk of developing type 2 diabetes are scarce and have generated conflicting results. Based on available clinical and epidemiological data, the positive effects of vitamin D seem to be primarily related to its action on insulin secretion and sensitivity and secondary to its action on inflammation. Future studies specifically designed to investigate the role of vitamin D on type 2 diabetes using inflammation as the main outcome are urgently needed in order to provide a more robust link between vitamin D, inflammation and type 2 diabetes.

Biological markers indicative of poor vitamin K status have been associated with a greater risk for hip fracture in older men and women. However, the dietary phylloquinone intake required to achieve maximal carboxylation of hepatic and extrahepatic vitamin K-dependent proteins is not known. In an 84-d study in a metabolic unit, 21 older (60-80 y) women were fed a phylloquinone-restricted diet (18 micro g/d) for 28 d, followed by stepwise repletion of 86, 200 and 450 micro g/d of phylloquinone. Plasma phylloquinone, urinary gamma-carboxyglutamic acid excretion and gamma-carboxylation of hepatic (prothrombin) and extrahepatic proteins (osteocalcin) decreased in response to phylloquinone restriction (P < 0.001), demonstrating the production of subclinical vitamin K deficiency. The gamma-carboxylation of prothrombin was restored to normal levels in response to phylloquinone supplementation at 200 micro g/d. In contrast, all other biochemical markers of vitamin K status remained below normal levels after short-term supplementation of up to 450 micro g/d of phylloquinone. These data support previous observations in rats that hepatic vitamin K-dependent proteins have preferential utilization of phylloquinone in response to phylloquinone dietary restriction. Moreover, our findings suggest that the current recommended Adequate Intake levels of vitamin K (90 micro g/d) in women do not support maximal osteocalcin gamma-carboxylation in older women.

Background: Adequate nutrition plays an important role in bone mass accrual and maintenance and has been demonstrated as a significant tool for the prevention of fractures in individuals with osteoporosis.