The hyperhomocysteinemia induced by a dietary addition of 1% methionine was significantly suppressed by the concurrent addition of 1% glycine or 1.4% serine to the same degree. The methionine-induced increase in the hepatic concentration of methionine metabolites was significantly suppressed by glycine and serine, but the hepatic cystathionine beta-synthase activity was not enhanced by these amino acids. When the methionine-supplemented diet was changed to the methionine plus glycine or serine diet, the plasma homocysteine concentration rapidly decreased during and after the first day. The hyperhomocysteinemia induced by an intraperitoneal injection with methionine was also suppressed by concurrent injection with glycine or serine, although the effect of serine was significantly greater than that of glycine. These results indicate that glycine and serine were effective for suppressing methionine-induced hyperhomocysteinemia: serine and its precursor glycine are considered to have elicited their effects mainly by stimulating cystathionine synthesis by supplying serine, another substrate for cystathionine synthesis.
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http://dx.doi.org/10.1271/bbb.60130 | DOI Listing |
Chem Res Toxicol
January 2025
Division of Laboratory Sciences, National Center for Environmental Health, Centers for Disease Control and Prevention, 4770 Buford Highway NE, Atlanta, Georgia 30341, United States.
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March 2025
The Shmunis School of Biomedicine and Cancer Research, The George S. Wise Faculty for Life Sciences, Sagol School of Neurosciences, Tel Aviv University, 6997801 Tel Aviv, Israel.
Dihydrolipoamide dehydrogenase (DLD) deficiency is an autosomal recessive disorder characterized by a functional disruption in several critical mitochondrial enzyme complexes, including pyruvate dehydrogenase and α-ketoglutarate dehydrogenase. Despite DLD's pivotal role in cellular energy metabolism, detailed molecular and metabolic consequences of DLD deficiency (DLDD) remain poorly understood. This study represents the first in-depth multi-omics analysis, specifically metabolomic and transcriptomic, of fibroblasts derived from a DLD-deficient patient compound heterozygous for a common Ashkenazi Jewish variant (c.
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January 2025
School of Basic Medical Sciences, Capital Medical University, Beijing 100069, China; Chinese Institute for Brain Research, Beijing 102206, China. Electronic address:
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January 2025
College of Animal Science and Technology, Qingdao Agricultural University, Qingdao 266000, China; Department of Biology and Agriculture, Zunyi Normal College, Ping`an Avenue, Hong Huagang District, Zunyi 563006, China.
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January 2025
State Key Laboratory of Food Science and Resources, Nanchang University, Nanjing Dong Lu 235, Nanchang 330047, China.
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