Vitamin K2 (Part 6): Osteocalcin & Diabetes – Another K2 Story?


I’ve shared with you a couple of times. I
I used to ignore vitamin K2. I totally ignored it for a long time. Then
some viewers asked me to look into it. So I did I went straight to the
clinical trials and there’s just not much on clinical trials on K2 yet. You
know, maybe there will be, maybe there won’t be. But recently, I got interested
yet again in vitamin K2 and I’m gonna drop that discussion for just a second
and pick up an entirely different thread and see if you start to make the
connection here. And again, this… there may be a significant connection, maybe not. Let me just read some titles. “Reduced
serum concentrations of carboxylated and undercarboxylated osteocalcin are
associated with the risk of developing type 2 diabetes.” The next one, “Osteocalcin
is related to enhanced insulin secretion in gestational diabetes.”
The third one, “Association between serum osteocalcin and markers of metabolic
phenotypes.” And when you get deeper into the article, the metabolic phenotypes,
they’re talking about are for a look for mostly insulin resistance, diabetes.
So there’s osteocalcin. Ring any bells? Let’s talk about that in just a minute.
But first… but before we do I mean there’s article after article “Low
osteocalcin level is a risk factor for impaired glucose metabolism in a Chinese
population.” And it just over and over and over again, this is… these are not two or
three articles that I’ve just cherry picked out of the science. There’s
clearly an implication for glucose metabolism linked to osteocalcin. Now
wait a minute. I just… osteocalcin ring any bells yet
for you? And to link it back to that first topic i brought up about vitamin
K2, remember we were talking about the mechanism how can vitamin K2 impact both
both soft tissue like artery walls and hard tissue bones. Well it has to do with
carboxylation. That’s undercarboxylated MGP and undercarboxylated osteocalcin with MGP matrix gla protein (MGP). That once you carboxylate
MGP, you can inhibit vascular calcification with the bone. You actually
you can increase calcification of the bone by carboxylating osteocalcin,
activating it. You can. Also, what most people don’t
don’t get into even the K2 Bureaus is that you can do… you can go
both ways in terms of calcium and bone. It helps to activate both osteoblasts
(which build or deposit bone calcium and bone) and osteoclasts (which cut calcium
or and/or protein out of the bone). But again, K2 is very involved in activation
of the enzymes which are involved, in turn, with managing calcium. So let’s go
one step further. As I mentioned, they just gives you the topic that I
covered just now. Osteoblasts, “B,” build. And osteoclast, “C,” cut. Both of
them have to do very much to do with bone mass. That’s how our body continues
to customize our bone mass to our current needs and again it’s MK7 is
suppresses on the osteoclast side and it stimulates on the osteoblasts side. So
very interesting, right? But wait a minute. Was this about K2 or was this about
insulin resistance? So in humans, osteocalcin levels are inversely
correlated with multiple various variables of type 2 diabetes such as
glucose intolerance and insulin resistance. Decreased levels of
osteocalcin have also been correlated with premature or myocardial infarction
and coronary heart disease. So here is a graph, looks kind of scatter shot at
first, but as you begin to notice, you don’t have a lot of dots down here and a
lot of dots up there. There is a fairly reasonable correlation. What is it?
Hemoglobin A1c on the vertical axis and osteocalcin on the horizontal axis so
it’s interesting I haven’t heard a lot of discussion about K2 and whether
there’s any at the end of the day whether there’s any K2 relationship with
insulin resistance and that’s one of the things that’s just really intriguing to
me right now. But as I said, there’s no question that
I’ll say that K2 is related to osteocalcin, and
osteocalcin is in turn related to insulin resistance. Here’s a visual on it.
Osteocalcin increases both adiponectin, adipocytes, fat cells, and proliferation
of beta cells, and increased insulin, and increased insulin sensitivity, leading to
improve glucose handling and lower fat mass. So what’s going on here? Uh heck if
I know but it’s a very interesting set of
relationships, isn’t it? If you’ve made it this far, thanks for your interest.

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