In addition to reproductive abnormalities, metabolic imbalances, especially
insulin resistance, characterize the core of PCOS pathology that, in turn, heightens the
existing hormonal dysregulation and possibly culminates in long-term complications
like type 2 diabetes and cardiovascular disorders. Insulin resistance is seen in most
people with PCOS. Insulin resistance in PCOS is due to post-receptor signaling defects
and is selective with attenuated metabolic and normal mitogenic pathways. It is also
probably tissue-selective. Insulin resistance alters the hypothalamic pituitary ovarian
axis and increases LH production greater than FSH. LH increases androgen production
from thecal cells of the ovary. Insulin resistance increases the risk of impaired glucose
tolerance, type 2 diabetes mellitus, obesity, cardiovascular disease, and dyslipidemia.
So, strategies for decreasing insulin resistance are important. Lifestyle intervention and
insulin sensitizers are in use in clinical practice for improving insulin sensitivity.
Further research is needed to develop newer therapeutics for insulin resistance.
Keywords: AMH, Androgen, Estrogen, FSH, Feedback, GnRH, Galanin, GABA, HPO, Hyperandrogenism, Insulin, Kisspeptin, LH, Leptin, Neurons, Ovarian, Opioid, PCOS, Progesterone, Secretion.
