The second hypothesis proposes that the signaling cascade for metabolic action of insulin in ovary becomes divergent from the one, which mediates steroidogenic action after binding of insulin to INSR.
In a subgroup of PCOS women, IR appears to be related to excess serine phosphorylation of the [beta] subunit of INSR (2).
Insulin and TZDs independently have been shown to increase expression of INSR, IRS-1, PPAR[gamma] and StAR protein in human ovarian cells (46).
The receptor kinase activity was optimal inspite of decrease in insulin induced INSR autophosphorylation suggesting a defect in signaling cascade between INSR and glucose transport (12).
CE decreased INSR mRNA levels in 3T3-L1 adipocytes (Cao et al.
cinnamon extract; DMEM, Dulbecco's modified Eagle's medium; GLUT, glucose transporter; GSK3B, glycogen synthase kinase 3 beta; GYS1, glycogen synthase 1; IGF, insulin-like growth factor; IGFR, insulin-like growth factor receptor; INS, insulin; INSR, insulin receptor; IRS, insulin receptor substrate; LEP, leptin; LEPR, leptin receptor; PIK3CB, phosphatidylinositol 3-kinase, catalytic, beta; PIK3R1, phosphatidylinositol 3-kinase, regulatory subunit 1; RPL32, ribosomal protein L32; SHC1, Src homology 2 domain-containing transforming protein 1; SOS1, Son of sevenless 1; TTP, tristetraprolin; ZFP36, zinc finger protein 36.