The development of diabetic peripheral neuropathy (DPN) is always followed by changes in vascular endothelial cells that are related to the reactivity of the homocysteine (Hcy) sulfhydryl group. In this meta-analysis, we investigated the association of Hcy with the pathogenesis and progression of DPN. We screened the Embase, Ovid, PubMed, Web of Science, Wangfang, and China National Knowledge Infrastructure databases.
Homocysteine (Hcy) is an independent risk factor of atherosclerosis through its involvement with the methionine cycle. In this study, we aimed to determine the blood vessel global methylation rate in Hcy-induced atherosclerosis in apolipoprotein-E-deficient (ApoE-/-) mice, and to explore the possible mechanism of this change in endothelial cells. ApoE-/- mice were divided into a hyperlipidemia (HLP) group, a hyperhomocysteinemia (HHcy) group, and an HHcy + folate + vitamin B12 (HHcy+FA+VB) group. Wild-type C57BL/6J mice were prepared as controls.
Association between neural tube defects (NTDs) and C677T polymorphism of the methylenetetrahydrofolate reductase (MTHFR) gene was suspected, because the MTHFR gene codes for a key enzyme in folate metabolism. Its deficiency usually leads to significant reductions in plasma concentrations of folate, vitamin B12 and methionine, whereas homocysteine levels are increased. We examined folate, vitamin B12 and homocysteine serum concentrations and polymorphism of the C677T MTHFR gene in Turkish children with neural tube defects.
Congenital heart defects (CHDs) are the most common birth defects; genes involved in homocysteine/folate metabolism may play important roles in CHDs. Methionine synthase reductase (MTRR) is one of the key regulatory enzymes involved in the metabolic pathway of homocysteine. We investigated whether two polymorphisms (A66G and C524T) of the MTRR gene are associated with CHDs. A total of 599 children with CHDs and 672 healthy children were included; the polymorphisms were detected by PCR and RFLP analysis.