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Glycine

Glycine, a non-essential amino acid, plays crucial roles in protein synthesis, neurotransmission, and DNA synthesis. Recent research has explored its potential to extend lifespan across various organisms, indicating that glycine supplementation may positively impact longevity through multiple mechanisms.

Glycine

PUBLICATIONS

  1. GlyNAC (Glycine and N-Acetylcysteine) Supplementation in Mice Increases Length of Life by Correcting Glutathione Deficiency, Oxidative Stress, Mitochondrial Dysfunction, Abnormalities in Mitophagy and Nutrient Sensing, and Genomic Damage.
          • Nutrients. 2022 Mar 7;14(5):1114.
          • Design: Study on C57BL/6J mice evaluating the effects of GlyNAC supplementation on lifespan and various age-associated defects.
          • Summary: GlyNAC supplementation in mice increased lifespan by 24% and corrected age-associated defects such as glutathione deficiency, oxidative stress, and mitochondrial dysfunction.
  2. Glycine supplementation extends lifespan of male and female mice.
          • Aging Cell. 2019 Jun;18(3):e12953.
          • Design: Study on genetically heterogeneous mice evaluating the effects of an 8% glycine diet on lifespan and pathology.
          • Summary: Glycine supplementation increased lifespan by 4%-6% and reduced the likelihood of death from pulmonary adenocarcinoma without increasing other pathologies.
  3. Glycine promotes longevity in Caenorhabditis elegans in a methionine cycle-dependent fashion.
          • PLoS Genet. 2019 Mar 7;15(3):e1007633.
          • Design: Study on Caenorhabditis elegans evaluating the effects of glycine supplementation on lifespan and its interaction with the methionine cycle.
          • Summary: Glycine supplementation prolonged lifespan in C. elegans by feeding into the methionine cycle, which is crucial for its longevity effects.
  4. Epigenetic regulation of the nuclear-coded GCAT and SHMT2 genes confers human age-associated mitochondrial respiration defects.
          • Sci Rep. 2015 May 22;5:10434.
          • Design: Study on human fibroblast lines derived from elderly subjects to examine the role of epigenetic regulation in age-associated mitochondrial defects.
          • Summary: Reprogramming elderly fibroblasts restored mitochondrial respiration defects through epigenetic regulation, and treatment with glycine prevented aging phenotypes.
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