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Dietary Kynurenine, the oxidized metabolite of tryptophan, suppresses osteoprogenitor expression of Hdac3 resulting in increased marrow adiposity and age‐related bone loss

Aging results in loss of skeletal bone mass resulting in osteoporosis and increased marrow fat although the mechanism remains poorly understood. Our previous studies support Hdac3 as a regulator of this process, as osteoprogenitor Hdac3 expression is decreased in aged vs. young mice, and decreased expression of Hdac3 causes an osteopenic, high marrow fat phenotype with increased lipid storage in osteoprogenitors. However, causative factors for decreased Hdac3 expression with aging are unknown. Our group has shown that aromatic amino acids (tyrosine, phenylalanine, tryptophan) function as antioxidants with a protective role in bone, whereas their oxidized byproducts antagonize this effect and promote bone loss. Circulating levels of kynurenine, the oxidized product of tryptophan, are increased in aged (24mo) vs. mature (12mo) mice, and we recently observed that kynurenine‐treated mice have high marrow fat and low bone mass, mimicking the phenotype of Hdac3‐deficient and aged animals. This raises the possibility that oxidized by products, in particular kynurenine, could be a mechanistic link between aging and bone loss.