Not exact matches
The most intriguing mutant type of mice were unusually thin; they generated more active
osteocalcin, secreted more insulin, and
produced many times more of the insulin - releasing cells in the pancreas.
To find out how, he turned to an engineered strain of mice lacking a gene for what was then a mysterious protein called
osteocalcin, which is
produced by osteoblasts.
Produced by our bones,
osteocalcin affects how we metabolize sugar and fat.
«When it is first
produced in osteoblasts,
osteocalcin is in an inactive form,» Ferron noted.
We naturally
produce less
osteocalcin throughout life as our bone mass declines.
The first protein is called
osteocalcin and is
produced in the bone by specialized cells charged with building bone called osteoblasts.
As mentioned above, genetic or pharmaceutical interventions to increase or decrease bone resorption not only controlled the release of undercarboxylated
osteocalcin, but also
produced the expected effects on energy metabolism and testosterone.
If this paradigm is correct, one could argue that adequate vitamin K is needed to ensure that
osteocalcin is fully carboxylated as it is
produced, allowing it to accumulate in bone matrix, so that the presence of the undercarboxylated form in the bloodstream accurately reflects the degree of bone resorption.
In older, non diabetic men, three years of supplementation with 500 micrograms / day of vitamin K1
produced a significant reduction in insulin resistance compared with controls.43 And in a study of healthy young men, just four weeks of supplementation with 30 mg of K2 three times daily improved insulin sensitivity.44 This may have occurred as a result of an increase in the vitamin K - dependent Gla - protein
osteocalcin, which has been shown in animal studies to increase insulin secretion and sensitivity.45