Dietary intake of phosphorus modulates the circadian rhythm in serum concentration of phosphorus. Implications for the renal production of 1,25-dihydroxyvitamin D.

Abstract

IntroductionWe recently reported that in healthy men, changes in the production rate (PR) (29), the serum concentration of 1,2540H)2D decreases. We have shown in healthy men that these phosphorus-induced changes in serum concentration of 1,25-(OH)2D can be accounted for entirely by changes in the production rate (PR) of the hormone (25). The mechanism by which changes in dietary phosphorus induce changes in the PR of 1,25-(OH)2D has, however, not been defined. In the chick and rat, the concentration ofphosphorus in serum (1 1, 19, 30, 31) or bathing medium (32) can be an important determinant of the activity of l-hydroxylase and the production rate of 1,25-(OH)2D. Yet, in humans, both restriction (24) and supplementation (25, 28) of dietary phosphorus can induce sustained changes in serum concentration of 1,25-(OH)2D without sustained changes in the morning fasting serum concentration ofphosphorus. These observations raise the question of whether changes in serum concentration of phosphorus do in fact mediate the changes in serum concentration of 1 ,2540H)2D induced by manipulation of dietary phosphorus.In normal subjects ingesting a normal diet, the serum concentration of phosphorus exhibits a circadian rhythm that is characterized by a nadir in the morning, a rise in early afternoon, and a peak at night (33-37). Indeed, Stanbury reported such a circadian rhythm in serum phosphorus in normal adult subjects ingesting only a small, constant amount of fluid hourly for 24 h (33). But Jubiz et al. subsequently reported that the nocturnal peak in serum phosphorus level was abolished in normal subjects receiving neither food nor fluid for 24 h, and suggested that the circadian changes in serum phosphorus were due in large part to food ingestion (35). In fact, it is not known whether the circadian rhythm in serum phosphorus can be affected by changes only in phosphorus intake in sub-

Effects of Phosphate Binders in Moderate CKD

“…In normal, healthy men given phosphorus-supplemented diets, single, fasting morning serum phosphorus concentrations grossly underestimate 24-hour exposure to phosphorus and fail to distinguish between low and high dietary phosphorus intake. 18 Our results suggest that, in moderate to advanced CKD, the serum phosphorus concentration may be a relatively poor marker of phosphate binder efficacy or adherence.…”

Assessing the Health Impact of Phosphorus in the Food Supply: Issues and Considerations

“…Figure 4 illustrates how both serum phosphate and PTH fluctuate with an inherent biphasic pattern, peaking in the afternoon and late evening but readjusting to the morning fasting concentration of the previous day (indicated by the arrows). This phenomenon of readjusting to the morning fasting concentration of the previous day has been shown for serum phosphate (16,(42)(43)(44), PTH (16,43), and, although less convincingly, FGF-23 (41,45). The need for multiple serum sampling to monitor dietary phosphorus effects on calcium and phosphorus balance was first suggested by Smith and Nordin in 1964 (42), when they were unable to demonstrate a change in serum calcium or phosphate concentrations in response to phosphorus intake using a single daily blood sampling.…”

“…Sampling during usual morning hours when study participants are in a fasted state, as is commonly done, will impair the ability to determine associations between dietary intake, phosphaturic hormones, and cardiovascular, renal, or skeletal disease biomarkers (16,34,(41)(42)(43)(44).…”

High phosphorus intake only slightly affects serum minerals, urinary pyridinium crosslinks and renal function in young women

“…Previous studies have demonstrated that, in order to counteract hyperphosphataemia, bioactive parathyroid hormone secretion is raised (Table 5; Reiss et al, 1970;Silverberg et al, 1986). However, hyperphosphatemia, induced by a high phosphorus intake, is associated with a decrease of 1,25-(OH) 2 D 3 concentration in the serum (Lobaugh, 1995;Portale et al, 1987). Contrary to this, Silverberg et al (1986) noticed no changes in 1,25-(OH) 2 D 3 concentrations (Table 5).…”