Serine is a nonessential amino acid used in protein biosynthesis and can be derived from four possible sources: dietary intake, degradation of protein and phospholipids, biosynthesis from glycolysis intermediate 3-phosphoglycerate, or from glycine.
Serine is found in soybeans, nuts, eggs, lentils, shellfish, and meats. Serine is used to synthesize ethanolamine and choline for phospholipids. Serine is essential for the synthesis of sphingolipids and phosphatidylserine in CNS neurons. In the folate cycle, glycine and serine are interconverted. These methyltransferase reactions and interconversions are readily reversible depending on the needs of the folate cycle. Dietary serine is not fully converted to glycine; therefore, serine supplementation has little value, though is not harmful.
Glycine and serine’s interconversion are important in mitochondrial glycolysis. Glycolysis provides ATP and energy in most cell types. Serine-glycine biosynthesis is a component in glycolysis-diverting pathways and nucleotide biosynthesis. This is clinically important, and specifically evident, in cancer. Cancer cells use glycolysis to sustain anabolism for tumor growth. Genetic and functional evidence suggests that abnormalities in the glycine-serine pathway represent an essential process in cancer pathogenesis by promoting energy production and promoting defective purine synthesis.
Serine is also a cofactor for the transsulfuration enzyme cystathionine-β-synthase making its availability important for glutathione production.
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Low serine may be due to decreased intake, or GI malabsorption and maldigestion. One pathway of serine biosynthesis requires the vitamin B6- dependent enzyme phosphoserine aminotransferase. With this, a functional need for vitamin B6 may contribute to low serine levels. Given its association with the folate cycle, plasma serine levels may be low or high with homocysteinemia and methylation defects; support with vitamin B6, B12, folate, or betaine can result in normalized homocysteine as well as serine.
High dietary intake of serine-rich foods, or supplementation, may result in elevated levels. Due to cofactors needed for serine metabolism, deficiencies of these nutrients can result in elevated serine levels. Administration of nutrients such as vitamin B6 or B1 have been shown to lower serine levels, as well as other amino acids.
Given its association with the folate cycle, plasma serine levels may be low or high with homocysteinemia and methylation defects; support with vitamin B6, B12, folate, or betaine can result in normalized homocysteine as well as serine.
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