Re: Can altered vascular permeability effect glocose levels?


"Insulin also increases the permiability of many cells to potassium,
magnesium and phosphate ions. The effect on potassium is clinically
important. Insulin activates sodium-potassium ATPases in many cells,
causing a flux of potassium into cells. Under certain circumstances,
injection of insulin can kill patients because of its ability to
acutely suppress plasma potassium concentrations.
http://www.vivo.colostate.edu/hbooks/pathphys/endocrine/pancreas/insulin_phys.html
"

"". In vitro and in vivo studies have demonstrated that insulin may
modulate the shift of Mg from extracellular to intracellular space.
Intracellular Mg concentration has also been shown to be effective in
modulating insulin action (mainly oxidative glucose metabolism), offset
calcium-related excitation-contraction coupling, and decrease smooth
cell responsiveness to depolarizing stimuli. A poor intracellular Mg
concentration, as found in noninsulin-dependent diabetes mellitus
(NIDDM) and in hypertensive patients, may result in a defective
tyrosine-kinase activity at the insulin receptor level and exaggerated
intracellular calcium concentration. Both events are responsible for
the impairment in insulin action and a worsening of insulin resistance
in noninsulin-dependent diabetic and
hhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12537988&dopt=Abstractypertensive
patients. "'

The above quotes indicate the Mg relations with insulin action. I think
lack of Mg may be related to calcium-related excitation-contraction
coupling, and decrease smooth cell responsiveness to depolarizing
stimuli....contracted conditions. ?? It may be important to understand
effect of hyperglycemia on mediating Mg defficiencies and
calcium-related excitation-contraction coupling, and decrease smooth
cell responsiveness to depolarizing stimuli...contracted condition.

.

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