Abstract

Abstract

Homocysteine (Hcy) is a sulfur-containing toxic amino acid derived from the metabolism of Methionine (Met). Hcy levels are broadly categorized as moderate (16 to 30 µmol/L), intermediate (31 to 100 µmol/L), and severe (over 100 µmol/L) [1]. Chronic elevation in Hcy concentration or its metabolites may cause Hyperhomocysteinemia (Hhcy) and Homocystinuria. Age, gender, family history of stroke, serum folate, vitamin B₁₂ deficiencies, and serum creatinine are important determinants of Hcy concentrations in the body [2, 3].  Hhcy is associated with an increased risk of diabetes, osteoporosis, cardiovascular disease, hip fracture, cognitive decline, chronic kidney disease, hypothyroidism, neurodegenerative disorders, oxidative stress, cancer, and dislocation of lenses [4, 5, 6]. In vitro study shows, Hhcy modulates the blood sugar levels in circulation and develops obesity [7, 8]. Hhcy is closely associated with the abnormality of Diabetes [9, 10, 11]. Vitamins B, Folate, and Choline are the key factors that regulate Hcy metabolic pathways. The supplementation of vitamins B₆, B₁₂, and folic acid has been clinically proven to lower Hcy levels in the circulation while the deficiencies in any of these vitamins might lead to an increased risk of Hcy concentration [12, 13, 14]. Hcy metabolism is also found linked to the genetic polymorphism of genes Methylene Tetrahydrofolate Reductase (MTHFR), Methionine Synthase (MTR), and Cystathionine β-Synthase (CBS) [15, 16, 17]. This study aims to establish the association of Hcy metabolism with obesity and osteoporosis.