High
dietary protein intake generates endogenous
acid production, which may adversely affect bone health. Alkaline
potassium citrate (Kcit)(2) may contribute to the neutralization of the
protein-induced
metabolic acidosis. We investigated the impact of 2 levels of
protein intake and Kcit supplementation on
acid-base metabolism and bone status in rats. Two-month-old Wistar male rats were randomly assigned to 4 groups (
n = 30 per group). Two groups received a normal-
protein content (13%) (NP) or a high-
protein (HP) content diet (26%) for 19 mo. The 2 other groups received identical diets supplemented with Kcit (3.60%) (NPKcit and HPKcit). Rats were pair-fed based on the ad libitum intake of the HP group. At 9, 16, and 21 mo of age, 10 rats of each group were killed. The HP diet induced a
metabolic acidosis characterized by
hypercalciuria, hypermagnesuria, and hypocitraturia at all ages. Kcit supplementation neutralized this effect, as evidenced by decreased urinary
calcium and
magnesium excretion by the HPKcit rats. Femoral bone mineral density, biomechanical properties, bone metabolism
biomarkers (
osteocalcin and
deoxypyridinoline), and plasma
insulin-like growth factor 1 levels were not affected by the different diets. Nevertheless, at 21 mo of age,
calcium retention was reduced in the HP group. This study suggests that lifelong excess of
dietary protein results in low-grade
metabolic acidosis without affecting the skeleton, which may be protected by an adequate
calcium supply.