The Effect of Time-Restricted Eating on Insulin Levels and Insulin Sensitivity in Patients with Polycystic Ovarian Syndrome: A Systematic Review

Figure 3

Illustration of the effect of hyperinsulinemia on insulin receptors and stimulation of steroidogenesis caused by hyperinsulinemia and increased LH (luteinizing hormone) levels. Insulin receptor defects are due to serine phosphorylation of the insulin receptor and IRS-1 (insulin receptor substrate 1) secondary to intracellular serine kinases. This results in reduced PI3K (phosphoinositide 3-kinase) downstream activity after insulin mediated activation and resistance to the metabolic actions of insulin. Activation of kinases in ERK/MAPK (extracellular signal-regulated kinases/mitogen-activated protein kinases) mitogenic pathway in PCOS (polycystic ovarian syndrome) causes inhibitory serine phosphorylation of IRS-1 in skeletal muscle in patients with PCOS as demonstrated here. These defects in the insulin receptor gene exist in patients with PCOS with extreme insulin resistance although insulin receptor numbers and affinity are similar to those in the patient without insulin receptor defects. Steroidogenesis is stimulated by both hyperinsulinemia causing inositolglycan generation and increased basal LH secreted from the anterior pituitary in response, also demonstrated below.