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Title: Dietary protein level and source differentially affect bone metabolism, strength, and intestinal calcium transporter expression during ad libitum and food-restricted conditions in male rats

Author
item GAFFNEY-STOMBERG, ERIN - Us Army Research Institute Of Environmental Medicine
item Cao, Jay
item LIN, GREGORY - Us Army Research Institute Of Environmental Medicine
item WULFF, CHARLES - Us Army Medical Research Institute
item MURPHY, NANCY - Us Army Medical Research Institute
item YOUNG, ANDREW - Us Army Medical Research Institute
item MCCLUNG, JAMES - Us Army Medical Research Institute
item PASIAKOS, STEFAN - Us Army Medical Research Institute

Submitted to: Journal of Nutrition
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/11/2014
Publication Date: 6/1/2014
Publication URL: http://handle.nal.usda.gov/10113/59614
Citation: Gaffney-Stomberg, E., Cao, J.J., Lin, G.G., Wulff, C.R., Murphy, N.E., Young, A.J., Mcclung, J.P., Pasiakos, S.M. 2014. Dietary protein level and source differentially affect bone metabolism, strength, and intestinal calcium transporter expression during ad libitum and food-restricted conditions in male rats. Journal of Nutrition. 144(6):821-829.

Interpretive Summary: High protein diets may attenuate bone loss induced by energy restriction (ER). We investigated whether high protein diets suppress bone turnover and improve bone quality during ER and whether dietary protein source affects this relationship in a rat model. Eighty 12-week old male Sprague Dawley rats were randomly assigned to eight treatment groups: 10% milk protein, 32% milk protein, 10% soy protein, or 32% soy protein under energy adequate (EA) or ER conditions (40% restriction). After 16 weeks, markers of bone turnover, bone mineral density (BMD) and structure, and expression of Ca channels in the duodenum were assessed. ER increased bone turnover and resulted in lower femoral trabecular bone volume and higher cortical bone surface compared to EA. High protein intake lowered bone turnover and tended to suppress PTH and increased trabecular BMD. Compared to milk protein, soy protein suppressed PTH, and increased cortical BMD and Ca content of the femur. During EA conditions, transient receptor potential cation channel, subfamily V, member 6 expression was higher for soy protein than milk protein and high protein compared to normal protein. These data demonstrate that both high protein and soy protein diets suppress PTH and high protein attenuates bone turnover and increases BMD regardless of energy status, likely due to enhanced intestinal Ca transporter expression.

Technical Abstract: High protein diets may attenuate bone loss during energy restriction (ER). The objective of the current study was to determine whether high protein diets suppress bone turnover and improve bone quality in rats during ER and whether dietary protein source affects this relationship. Eighty 12-week old male Sprague Dawley rats were randomized to receive one of 4 study diets: 10% milk protein (CP-MP), 32% milk protein (HP-MP), 10% soy protein (CP-SP), or 32% soy protein (HP-SP) under energy adequate (EA) or ER conditions (40% restriction). After 16 weeks, markers of bone turnover, bone mineral density (BMD) and structure, and expression of Ca channels in the duodenum were assessed. ER increased bone turnover and resulted in lower femoral trabecular bone volume (P < 0.05) and higher cortical bone surface (P < 0.001) compared to EA. High protein intake lowered bone turnover and tended to suppress PTH (P = 0.06) and increased trabecular BMD (P < 0.05) compared to CP. Compared to MP, SP suppressed PTH (P < 0.05), and increased cortical BMD (P < 0.05) and Ca content of the femur (P < 0.01). During EA conditions, transient receptor potential cation channel, subfamily V, member 6 expression was higher for SP than MP (P < 0.05) and HP compared to CP (P < 0.05). These data demonstrate that both HP and SP diets suppress PTH and HP attenuates bone turnover and increases BMD regardless of energy status. These findings may be due in part to enhanced intestinal Ca transporter expression.