(not all men / women having insulin
resistance) use inositol phosphoglycan
mediators , AS such if there is a deficiency of the d-chiro-inositol
phosphoglycan mediator then the action of insulin may result in resistance to
insulin in a subset of PCOS women, but not all cases.
Some men
& women may involve
low-molecular-weight inositol phosphoglycan mediators as a second pathway for entry
of glucose in cells . When insulin binds to such kind of uncommon receptor, mediators of this class(Myo inositol
/DCI driven pathway of cell) are generated by hydrolysis of glycosyl-phosphatidyl-inositol
lipids located at the outer leaflet of the cell membrane. Released mediators
are then internalized and affect intracellular metabolic processes. Although different species (about seven types if I
remember correctly) have been identified, an inositol phosphoglycan molecule
containing d-chiro-inositol and galactosamine is known to have a role in
activating key enzymes that control the oxidative and non-oxidative metabolism
of glucose. Therefore a deficiency of the d-chiro-inositol
phosphoglycan mediator of the action of insulin may result in resistance to
insulin. Insulin resistance has been linked to decreased urinary excretion
of chiro-inositol (a component of the putative d-chiro-inositol
phosphoglycan mediator) in humans with impaired glucose tolerance.
Few decades
back , in animal studies it has been shown that administration of d-chiro-inositol
decreased hyperglycemia in rats with diabetes and improved glucose tolerance in
normal rats, such was also the results monkeys with varying degrees of insulin
resistance, d-chiro-inositol accelerated the disposal of glucose and
decreased insulin secretion. Therefore it is logical to believe
That d-chiro-inositol, by virtue of its ability to
increase sensitivity to insulin, would have beneficial effects on ovulation and
ovarian production of androgens in women with the polycystic ovary syndrome.
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