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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

Erin Gaffney-Stomberg, Jay J. Cao, Gregory G. Lin, Charles R. Wulff, Nancy E. Murphy, Andrew J. Young, James P. McClung, Stefan M. Pasiakos
Journal of nutrition 2014 v.144 no.6 pp. 821-829
animal models, biomarkers, bone density, bone resorption, calcium, calcium channels, dairy protein, dietary restriction, duodenum, energy, femur, high protein diet, low calorie diet, protein intake, protein sources, rats, soy protein
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.