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Vitamin K Helps in Regulating Insulin Activity in Diabetes
Posted: Thursday, August 23, 2007
The vitamin K dependant protein osteocalcin may have a positive effect on reducing obesity and diabetes, suggests a new study.
Researchers studied the effect bone cells have in energy regulation, and found that osteocalcin plays a key role in regulating insulin activity.
There are two main forms of vitamin K: phylloquinone, also known as phytonadione, (vitamin K1) which is found in green leafy vegetables such as lettuce, broccoli and spinach, and makes up about 90 per cent of the vitamin K in a typical Western diet; and menaquinones (vitamin K2), which make up about 10 per cent of Western vitamin K consumption and can be synthesized in the gut by microflora.
The study points to another potential avenue for vitamin K - a vitamin which is less known than vitamins A to E - and could help diversify its health benefits, which have previously been linked to cardiovascular health and bone health.
Previous animal studies have thrown up interesting results at high dose supplementation of vitamin K and its effect on arterial calcification.
Both K1 and K2 have been shown to play a role in bone health, influencing the secondary modification of osteocalcin, a protein needed to bind calcium to the bone matrix. Some large human studies have tested the bone health benefits of calcium alone, calcium plus vitamin D and calcium plus vitamin D plus vitamin K. The latter has been reported to show the best effect on osteoporosis.
In this animal study, researchers from America, Canada and Britain identified the genes that operate primarily in the bone cells that are linked to glucose metabolism. By "knocking out" these genes in mice so that they could not function, the animals lacking a functional osteocalcin gene gained fat, showing that osteocalcin helps regulate the cells that produce insulin in the pancreas and release it into the bloodstream.
These osteocalcin deficient mice also became glucose intolerant. Both conditions are considered "pre-diabetic." Osteocalcin was also shown to signal fat cells to release a hormone called adiponectin that increases insulin sensitivity.
"We show here that mice lacking the protein tyrosine phosphatase OST-PTP are hypoglycemic and are protected from obesity and glucose intolerance because of an increase in b-cell proliferation, insulin secretion, and insulin sensitivity. In contrast, mice lacking the osteoblast-secreted molecule osteocalcin display decreased b-cell proliferation, glucose intolerance, and insulin resistance," the researchers wrote.
They added: "Ex vivo, osteocalcin can stimulate CyclinD1 and Insulin expression in b-cells and Adiponectin, an insulin-sensitizing adipokine, in adipocytes; in vivo osteocalcin can improve glucose tolerance.
"By revealing that the skeleton exerts an endocrine regulation of sugar homeostasis this study expands the biological importance of this organ and our understanding of energy metabolism."
Source: Diabetes In Control: Cells Published on-line, doi:10.1016/j.cell.2007.05.047. "Endocrine Regulation of Energy Metabolism by the Skeleton" Authors: Na Kyung Lee, Hideaki Sowa, Eiichi Hinoi, Mathieu Ferron, Jong Deok Ahn, Cyrille Confavreux
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