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ARS Home » Southeast Area » Little Rock, Arkansas » Microbiome and Metabolism Research Unit » Research » Publications at this Location » Publication #266728
Title: Effects of Nutrition and Alcohol Consumption on Bone Loss

Author
item RONIS, MARTIN - Arkansas Children'S Nutrition Research Center (ACNC)
item MERCER, KELLY - Arkansas Children'S Nutrition Research Center (ACNC)
item CHEN, JINRAN - Arkansas Children'S Nutrition Research Center (ACNC)

Submitted to: Osteoporosis Report
Publication Type: Review Article
Publication Acceptance Date: 1/25/2011
Publication Date: 3/1/2011
Citation: Ronis, M.J., Mercer, K., Chen, J. 2011. Effects of Nutrition and Alcohol Consumption on Bone Loss. Osteoporosis Report. 9(2):53-59.

Interpretive Summary: This review article summarizes the most recent literature on the effects of diet and chronic alcohol on the skeleton. Results discussed include new studies on reduced bone quality produced by obesity; bone-loss in alcoholics produced by direct effects of ethanol on bone cells and indirect effects of ethanol on bone associated with endocrine disruption through the parathyroid hormone and growth hormone axis; and studies on bone promoting actions of fruits and soy products. New findings highlighted include inhibitory actions of obesity-associated free fatty acids and of ethanol on bone formation and increased generation of bone marrow fat through altered signaling by Wnt and PPAR'gamma transcription factors. In addition, the role of oxidative stress in stimulation of bone loss through increased bone resorption is discussed. Increased bone formation after feeding fruits (prunes/blueberries) or soy products is discussed in the context of effects on Wnt and bone morphogenic protein signaling.

Technical Abstract: It is well established that excessive consumption of high fat diets results in obesity. However, the consequences of obesity of skeletal development, maturation and remodeling have been the subject of controversy. New studies suggest that the response of the growing skeleton to mechanical loading is impaired and trabecular bone mass is decreased in obesity and after high fat feeding. At least in part, this occurs as a direct result of inhibited Wnt signaling and activation of PPAR'gamma pathways in mesenchymal stem cells by fatty acids. Similar effects on Wnt and PPAR gamma signaling occur after chronic alcohol consumption as the result of oxidative stress and result in inhibited bone formation accompanied by increased bone marrow adiposity. Alcohol-induced oxidative stress as the result of increased NADPH-oxidase activity in bone cells also results in enhanced RANKL-RANK signaling to increase osteoclastogenesis. In contrast, consumption of fruits and legumes such as blueberries and soy increase bone formation. New data suggest that Wnt and BMP signaling pathways are the molecular targets for bone anabolic factors derived from the diet.