Role of insulin and insulin resistance in androgen excess disorders

Table 1 Studies demonstrating cellular mechanisms of insulin resistance in women with polycystic ovary syndrome

Ref.	Objective	Method(s)	Main result(s)	Conclusion
Dunaif et al[22]	To investigate the cellular mechanisms of insulin resistance in PCOS.	Cultured skin fibroblasts from 14 women.	Increased serine phosphorylation and reduced tyrosine phosphorylation of insulin receptor.	One of the mechanisms of insulin resistance at the receptor level was demonstrated. However, 50% of women did not show this abnormality, indicating heterogeneity in the pathogenesis of insulin resistance in PCOS.
Book and Dunaif[23]	To explore the mechanisms of the paradox in metabolic and mitogenic actions of insulin.	Metabolic and mitogenic actions of insulin and IGF-1 were evaluated in cultured skin fibroblasts of 16 PCOS and 11 control women.	No difference in the number and affinity of insulin receptor in either group. Decreased glucose incorporation into glycogen in women with PCOS.Thymidine incorporation was similar between the groups.	Women with PCOS show decreased metabolic action but mitogenic action of insulin signaling was similar between the groups.
Belani et al[24]	To unravel insulin and steroidogenic signaling pathways in PCOS.	Insulin receptor beta subunit expression was investigated in luteinized granulosa cells obtained from 30 healthy women and 39 women with PCOS.	Compared to controls, 64% of cells show reduced insulin receptor beta subunit expression.Insulin-resistant women also showed decreased PI3 kinase expression.	Lower viability of luteinized granulosa cells in insulin-resistant women with PCOS.

PCOS: Polycystic ovary syndrome; IGF-1: Insulin-like growth factor-1; PI3 kinase: Phosphatidylinositol-3-kinase.