Inositolphosphoglycans (IPGs) as mediators of insulin's steroidogenic actions.
PCOS is a unique model of insulin resistance in which one tissue (skeletal muscle) is resistant to insulin in terms of glucose metabolism whereas another tissue (ovarian thecal cells) maintains its responsiveness to insulin in terms of testosterone biosynthesis. During the past decade, a series of in vitro studies conducted in human placental cells /25/, swine granulosa cells /28/, and most recently, human thecal cells /17/, have provided compelling evidence that one factor involved in this apparent clinical paradox is the clear demonstration of the utilization of the IPG signal transduction system for insulin's effects on steroidogenesis. Nonetheless, many questions remain to be addressed. For example, it would be instructive to determine simultaneously the effects of insulin on glucose disposal and testosterone biosynthesis in isolated thecal cells. In other words, is the thecal cell itself resistant to insulin in terms of glucose disposal while remaining sensitive to insulin in terms of testosterone biosynthesis? Is the IPG content of human thecal cells from women with PCOS decreased compared with that in matched healthy women? There is substantial evidence to suggest that some IPGs may also be responsible in part for mediating insulin's stimulation of glucose disposal (see paper by Dr. Joseph Larner in this issue)--this raises the question as to whether specific forms of IPGs are responsible for glucose metabolism in vivo, whereas other IPGs are responsible for mediating insulin's effects on steroidogenesis. Is there a disparity in the ratio of different types of IPGs among various tissues (e.g., muscle, liver, ovary), and does that ratio determine the tissue's responsiveness to one or another action of insulin? These questions and others leave IPGs and insulin signal transduction a fruitful area for both clinical and laboratory investigations.[1]References
- Inositolphosphoglycans (IPGs) as mediators of insulin's steroidogenic actions. Nestler, J.E. Journal of basic and clinical physiology and pharmacology. (1998) [Pubmed]
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