The effects of dietary acid stress on bone metabolism in young ovariectomized and intact rats

Abstract

1.Two studies were performed to determine the effects of acid stress and ovanectomy on bone metabolism in young rats. In Expt 1, eighteen female weanling Sprague-Dawley-descended rats were ovariectomized, placed in one of three dietary groups and given a diet containing (g/kg): 6 calcium and 3. 6 or 12 phosphorus for 10 weeks. In Expt 2, thirty-two female weanling Sprague-Dawley-descended rats were ovariectomized, and thirty-two were left intact. Eight rats from each group were given a diet containing (g/kg): 6 Ca and 3 P, 12 P, 3 P+ 1 S or 3 P+20 ammonium chloride for 10 weeks.2. Feeding diets containing 12 g P/kg resulted in decreased serum Ca and increased urinary P with no changes in femur composition. Feeding high-sulphate and ammonium chloride diets resulted in increased urinary Ca and, when combined with ovariectomy, lower femur Ca and P with no changes in femur hydroxyproline or hexosamines.3 . The findings reflect the more rapid turnover of the amorphous calcium phosphate salts found in greater amounts in bones of younger animals than for more stable apatitic crystals that predominate in bones of older animals.

Nutrition and the growth and racing performance of thoroughbred horses

“…The rise in urinary N is likely to be associated with increased urinary sulphur and phosphorus which could increase urinary calcium loss (Frape, 1987) as observed by Glade et al (1985). Similar observations were made in acid-stressed rats (Kunkel et al 1986). Excessive protein consumption superimposed on training diets frequently found to contain too much P and too little Ca could aggravate existing bone disorders.…”

Bone Mineral Crystallinity Governs the Orchestration of Ossification and Resorption during Bone Remodeling

“…A major paradigm dispelled by this model is that an ideal bone regeneration therapy is such that it augments osteogenesis and hinders the osteoclastic resorption, when, in fact, the healthy composition and architecture of bone depend on the optimal orchestration of these two antagonistic processes. This explains why the bone mineral is poorly crystalline and also why the proportion of ACP in bone steadily decreases with age, − paralleling the age-related loss of bone flexibility and deterioration of bone health. With the aid of linear logic, we may be tempted to think that proneness to conditions such as rickets or osteoporosis is paralleled by the higher amount of ACP in bone and a greater solubility of the bone mineral that this would entail.…”