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Effects of thermal and enzymatic treatments of soybean meal on apparent absorption of total phosphorus, phytate phosphorus, nitrogen (protein), ash, calcium, magnesium, copper, iron, manganese, strontium and zinc were examined using rainbow trout, Oncorhynchus mykiss (Walbaum), as the test species. Absorption of the test nutrients was estimated using yttrium as an inert non‐absorbable indicator. Thermal treatments (microwaving, dry roasting, steam heating, cooking) had no measurable effect on the apparent absorption of phosphorus and other minerals. Phytase supplementation increased the apparent absorption of phosphorus, nitrogen (protein), ash, calcium, magnesium, copper, iron, strontium and zinc in low‐ash diets containing soybean meal, but had little effect in high‐ash diets containing both soybean and fish meal. In low‐ash diets, the apparent absorption of phosphorus increased in accord with the level of phytase added to the diet, from 27% (no phytase added) up to 90% (phytase added, 4000 units kg−1 diet) or 93% (predigested with phytase, 200 units kg−1 soybean meal). In high‐ash diets, dietary acidification with citric acid decreased the effect of phytase, whereas in low‐ash diets, acidification markedly increased the effect of the enzyme. Excretion of phosphorus in the faeces of fish fed a low‐ash diet containing phytase‐treated soybean meal was 0.32 g per kg diet consumed, a 95%−98% reduction compared with phosphorus excretion by fish consuming commercial trout feeds.

Phosphorus (P) is an essential component of fish diets. Its deficiency affects not only hard tissues, where it is responsible for rickets, leading to skeletal malformation, but also influences various aspects of intermediary metabolism, and thus growth and feed conversion. Therefore, optimizing the dietary inclusion level is critical at all times. As the aquaculture industry has expanded, so the effects of P in farm effluents, derived from metabolic and uneaten food sources, have also become recognized. Diets are increasingly formulated on a basis that will not only provide adequate P for fish needs, but also endeavour to ensure minimal acceptable P levels in effluents at the same time. Many variables influence P requirements and P availability in fish diets, so it is inadvisable to feed diets formulated to an assumed minimum dietary requirement level, irrespective of the advantages that such a formulation may provide to environmental impact.

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The apparent digestibilities (availabilities) of dry matter, protein, phosphorus and selected minerals in fish and animal by‐products were determined using rainbow trout Oncorhynchus mykiss (Walbaum). Blood meal (ring‐dried), feather meal and deboned fish meal had relatively high concentrations of protein, low concentrations of phosphorus and many minerals, and high digestibilities (availabilities) of these nutrients. Other animal by‐products, however, had high concentrations of minerals, including phosphorus, which are associated with the bone fraction. Availabilities of manganese and zinc in the diet were reduced by the inclusion of high‐ash animal by‐products in the diet, whereas availabilities of potassium, sodium and copper were relatively unaffected. Dietary concentrations of bone minerals (calcium, phosphorus) and ash were inversely correlated with availabilities (% of intake) of most minerals except copper in the diet. Also, dietary concentrations of bone minerals correlated inversely with the net absorption (mg g−1 diet) of zinc, manganese and magnesium in the diet. When rainbow trout were fed diets containing incremental concentrations of fish bones, the apparent availabilities of phosphorus, calcium, magnesium and iron decreased as fish bone content in the diet increased. Reducing the bone fraction of high‐ash (high‐phosphorus) by‐product meals is therefore an essential approach to using such ingredients in low‐pollution fish feeds.

Renal disease leads to perturbations in calcium and phosphate homeostasis and vitamin D metabolism. Dietary fructose aggravates chronic kidney disease (CKD), but whether it also worsens CKD-induced derangements in calcium and phosphate homeostasis is unknown. Here, we fed rats diets containing 60% glucose or fructose for 1 mo beginning 6 wk after 5/6 nephrectomy or sham operation. Nephrectomized rats had markedly greater kidney weight, blood urea nitrogen, and serum levels of creatinine, phosphate, and calcium-phosphate product; dietary fructose significantly exacerbated all of these outcomes. Expression and activity of intestinal phosphate transporter, which did not change after nephrectomy or dietary fructose, did not correlate with hyperphosphatemia in 5/6-nephrectomized rats. Intestinal transport of calcium, however, decreased with dietary fructose, probably because of fructosemediated downregulation of calbindin 9k. Serum calcium levels, however, were unaffected by nephrectomy and diet. Finally, only 5/6-nephrectomized rats that received dietary fructose demonstrated marked reductions in 25-hydroxyvitamin D 3 and 1,25-dihydroxyvitamin D 3 levels, despite upregulation of 1␣-hydroxylase. In summary, excess dietary fructose inhibits intestinal calcium absorption, induces marked vitamin D insufficiency in CKD, and exacerbates other classical symptoms of the disease. Future studies should evaluate the relevance of monitoring fructose consumption in patients with CKD.

A new method was developed to estimate the minimum dietary requirement of phosphorus (P) for large fish for which conventional methods are not suitable. The method is based upon nonfecal (mainly urinary) excretion of inorganic P and total nitrogen from fish placed in a metabolic tank. In the first experiment, small and large rainbow trout (body wt 203 and 400 g, respectively) and, in the second experiment, P-sufficient, P-deficient and starved rainbow trout (different in diet history; body wt 349-390 g) were fed a constant amount (standard feeding rate) of semipurified diets with incremental P concentrations once daily at 15 degrees C. In all cases, there was no measurable excretion of P when dietary P concentration was low; however, beyond a specific dietary concentration, excretion of P increased rapidly. The point where the fish started to excrete P was assumed to be the minimum dietary requirement. By d 3 of consuming the experimental diets, the response of the fish to dietary P concentration stabilized, and excretion of P remained constant within dietary treatment groups for the subsequent sampling days (d 6, 9 and 12). The minimum dietary requirement of available P for fish having body wt of 203 and 400 g was estimated to be 6.62 and 5.54 g/kg dry diet, respectively, and that for P-sufficient, P-deficient and starved fish was estimated to be 4.06, 5.83 and 4.72 g/kg dry diet, respectively, when feed efficiency is 1.

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