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ARS Home » Southeast Area » Little Rock, Arkansas » Microbiome and Metabolism Research Unit » Research » Publications at this Location » Publication #296561

Title: Molecular mechanisms underlying the actions of dietary factors on the skeleton

item RONIS, MARTIN - Arkansas Children'S Nutrition Research Center (ACNC)

Submitted to: Book Chapter
Publication Type: Book / Chapter
Publication Acceptance Date: 6/15/2011
Publication Date: 1/15/2013
Citation: Ronis, M.J.J. 2013. Molecular mechanisms underlying the actions of dietary factors on the skeleton. In: Watson, R.R., Preedy, V.R., editors. Bioactive Foods as Dietary Interventions of the Aging Population. Elsevier Ltd., U.K. p. 421-432.

Interpretive Summary:

Technical Abstract: This book chapter summarizes the current state of knowledge on molecular mechanisms whereby nutritional status and dietary factors found in fruits, vegetables, and grains affect bone turnover and skeletal quality. The Wnt-beta catenin and bone morphogenic protein (BMP) pathways in osteoblast bone cell precursors are identified as critical targets for berries and soy foods, respectively. These converge on the transcription factor Runx2 which is critical for normal development of bone marrow stem cells into bone. Estrogens suppress bone turmover in part as a result of inhibition of the RANKL/RANK signaling pathway which is essential for formation of bone resorbing osteoclast cells. Estrogens also protect mature osteoblast bone cells from death/senescence as a result of interactions with oxidant/antioxidant and inflammatory signaling in bone cells. Evidence for and against the action of soy diets on estrogen receptor signaling pathways is discussed in light of the natural presence of phytoestrogens genistein and daidzein in soy. In addition, the effects of antioxidant/anti-inflammatory drugs on bone loss associated with aging, alcohol abuse, and arthritis is discussed together with the potential for antioxidant/anti-inflammatory actions associated with fruit and vegetable consumption. Finally high-fat diet-associated obesity has been shown to result in bone loss and increased fracture risk. The mechanisms underlying this effect are discussed in relationship to activation of the transcription factor PPAR gamma by fatty acids and their metabolites. PPAR gamma-activation results in diversion of bone marrow stem cells into fat cells instead of bone cells and accumulation of fat in bone marrow with accompanying loss of skeletal integrity.