insulin mimics?

anon said:

Can someone explain how insulin mimics, like vanadium, lipoic acid, or cinnamon, do not have the
negative effects of insulin?

Because insulin mimic is a misleading term. They don't do the same thing as insulin, rather they
have cellular effects that make the process of insulin-stimulated glucose uptake work better. This
can be by inhibiting enzymes that deactivate insulin receptors, or by acting as antioxidants that
prevent damage, or in a number of other indirect ways. The result is increased glucose uptake, but
not by acting as if they were insulin.

Quoted message said:

I guess the idea is that a mimic is doing some of the good parts of what insulin does, but not the
bad parts.

Since the different roles of insulin are due to it acting on different proteins, it's always
possible that a molecule which activates one insulin target, won't activate another. Adrenaline
activates two types of receptor - alpha and beta - which recognize a different part of the
adrenaline molecule. It's therefore possible to develop a drug that will block adrenaline's function
via alpha receptors, while leaving its functions via beta receptors unchanged.

MattLB

anon said:

Can someone explain how insulin mimics, like vanadium, lipoic acid, or cinnamon, do not have the
negative effects of insulin?

What negative effects are you thinking about?? I find there is a lot of misunderstanding on what
insuline does. But I think that happens because most peope think of insuline as a single regulator
of glucose. While it is only one part of a multidirectional regulation system, where at least one
other component, glucagon, is part of the same story. Diabetes can also be that glucagon is
misregulated, eg. is firing constantly, instead of being quenched by insulin release. The third part
might be amylin, a fourth part somatostatin. And to confuse the whole picture, stomach lining and
intestine lining has Alfa cells releasing glucagon alike peptides, which do not increase sugar
release, but seem to rather increase insulin release sensitivity.

If insuline quenche glucagon release too heavily, the glucagon release will start too late when
glucose fall is on the strongest, and the undershoot in blood glucose may be too big and a strong
hypoglucaemia may result. Another signal that may hamper both insuline release and glucagon release
is somatostatin release which curiously enough quench both releases. Maybe somatostatin release may
be a vicious one in diabetics ??

Oh, by the way, it seems that also glucagon release quench insuline release too. doing so should be
rather natural. Whom of you run the refigerator and the heater in your air condition system at the
same time?? It happens, but then only the electricity delivers are glad in order to sell you lot of
electricity to feed the vicious cycle. The heater heats of the cooled air and the cooler cools the
heated air :-) If both insuline and glucagon are released in parallell, they just contradict each
other and glucose level would be anywhere, depending on what will dominate. In T2 diabetics, it is
reported to happen, and at such rates of glucagon that glucose never falls below 12-15 mmol/l.

And by the way, both adrenaline and TNF-alpha may release glucagon while it shouldn't.

And, adrenaline is released in stress situation, TNF-alpha is released by adipocytes when they need
more fuel, and also by lymphocytes etc. in order to make more sugar available to immune system in
infections, like periodintitis and chronic inflammation in teeth root channels, like I had and
other chronic inflammations wherever in body. So, by coincidence, chronic inflammations in teeth
and gum from increased glucose usages in food may induce abnormal glucagon release and make fat
cells make more more fat from the released glucose not needed at all by neither immune system,
neither muscles, only by some few lymphocytes in gum who are overstimulated by infection and free
radical production locally.

MattLB said:

Because insulin mimic is a misleading term. They don't do the same thing as insulin, rather they
have cellular effects that make the process of insulin-stimulated glucose uptake work better. This
can be by inhibiting enzymes that deactivate insulin receptors, or by acting as antioxidants that
prevent damage, or in a number of other indirect ways. The result is increased glucose uptake, but
not by acting as if they were insulin.

Do you know if any has done some research if Vanadium could bind to chromomoduline and be just as
effective as Cr III in potentiating insuline stimulation effectiveness. By satiating chromomoduline
with Cr III, it potentiates insuline stimulating effectiveness by a factor of around 10, while
partially binding even can inhibit effectiveness. The daily need to bind all 6 atoms to
chromomoduline has been proposed to be around 600 ug Cr II daily. While Cr pills only has 100 ug.

Alf Christophersen said:

MattLB said:

Because insulin mimic is a misleading term. They don't do the same thing as insulin, rather they
have cellular effects that make the process of insulin-stimulated glucose uptake work better.
This can be by inhibiting enzymes that deactivate insulin receptors, or by acting as antioxidants
that prevent damage, or in a number of other indirect ways. The result is increased glucose
uptake, but not by acting as if they were insulin.

Do you know if any has done some research if Vanadium could bind to chromomoduline and be just as
effective as Cr III in potentiating insuline stimulation effectiveness.

The mode of action of vanadium and chromium are quite different AFAIK, (enzyme inhibitor versus
enzyme/receptor enhancer) and Pubmed gives no hits.

Quoted message said:

By satiating chromomoduline with Cr III, it potentiates insuline stimulating effectiveness by a
factor of around 10, while partially binding even can inhibit effectiveness. The daily need to
bind all 6 atoms to chromomoduline has been proposed to be around 600 ug Cr II daily. While Cr
pills only has 100 ug.

Interestingly chromium picolinate, the standard form of supplement is such a strong complex that it
doesn't release the chromium ions at an appreciable rate under most physiological conditions. In
addition the redox state of the chromium is shifted to one in which it can react to form hydroxyl
free radicals.

MattLB