Abstract
Homocysteine is an intermediate substance formed during the breakdown of the amino acid methionine and may undergo remethylation to methionine or trans-sulfuration to cystathionine or cysteine. The metabolism occurs via two pathways: remethylation to methionine, which requires folate and vitamin B12; and transsulfuration to cystathionine, which requires pyridoxal-5’-phosphate. The disturbances in the metabolic pathways lead to the accumulation of Hcy, either by insufficient transsulfuration (through CBS mutations or vitamin B6 deficiency) or by a blockage of remethylation. In the latter case, folate or vitamin B12 deficiency may be involved, as well as MTHFR. High levels of Hcy induce sustained injury of arterial endothelial cells, proliferation of arterial smooth muscle cells and enhance activity of key participants in vascular inflammation, atherogenesis, and vulnerability of the established atherosclerotic plaque. Hyperhomocysteinemia has become the topic of interest in recent years. It has been highly associated with increased risk for cardiovascular disorders, such as, atherosclerosis, thromboembolism and dyslipidemia. Women with PCOS show constellation of metabolic syndromes. Obesity, hyperandrogenemia and type 2 diabetes mellitus is the hallmark of PCOS which later becomes the risk factors for cardiovascular disease. Various studies had revealed the presence of increased Hcy level in PCOS women which may or may not be associated with other biochemical parameters. Intense treatment for PCOS can influence homocysteine levels.
Highlights
A case-control study conducted in the year 2016 showed that the serum homocysteine levels were significantly high in Polycystic ovary syndrome (PCOS) women
Recent research by Sachan Rekha et al have reported significant higher serum Homocysteine HOMA-IR (Hcy) level in PCOS women, remarkably increased in both obese and non-obese PCOS women and it was best correlated with HOMA-IR out of three indices used for IR [23]
Insulin and Hcy have the ability to induce each other by inhibiting hepatic Cystathionine Beta Synthase E2 (CBS) [23] that results in hyperhomocysteinemia leading to compensatory hyperinsulinemia by inducing insulin resistance
Summary
The constellations of symptoms significantly affect the quality of life of PCOS women and the syndrome is associated with an increased long term risk factors such as cardiovascular disease, diabetes mellitus, infertility, cancer and psychological disorders [10]. Homocysteine, a biosynthesis of methionine has proved as a major cardinal feature of PCOS. It is a non-protein a-amino acid and cysteine homologue. A condition that emerges from disrupted homocysteine metabolism is hyperhomocysteinemia which has been known as the most significant risk factor for cardiovascular disease and has been confirmed by recently conducted meta-analysis study by Homocysteine Studies Collaboration [13]. Deficiencies in cystathionine beta synthase, methylenetetrahydrofolate reductase or enzymes involving methyl-B12 synthesis, as a result of a rare genetic defect, lead to severe hyperhomocysteinemia.
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