Review: Phosphorus in Fish Nutrition

anti-rachitic property. McCollum, therefore, named this factor vitamin D. McCollum's demonstration, however,
was incomplete for Mellanby. Thus, Mellanby argued that there was no guarantee that the oxidation of cod liver
oil completely destroyed vitamin A. A trace amount of vitamin A, which could remain in the oxidized oil, might
not be enough to prevent xerophthalmia, but enough to cure rickets.
Vitamin D and P utilization
Research on vitamin D is very diverse. This section presents only a cursory review of vitamin D research relat ed to
P utilization. A pioneer research on vitamin D can be traced back to Mellanby (1919). But, a substantial number
of researches or observations on cod liver oil and rickets had been reported much earlier. They were already
mentioned in the previous chapters. Kramer & Howland (1932) concluded that with minimal amount of vitamin
D, the Ca and P of the serum of rats varied directly with the Ca and P concentrations in the diet, and that vitamin D
stabilized the Ca and Pi concentrations in the serum. Hannon et al. (1934) administered a small amount of vitamin
D 2 over a period of 16 days to a patient suffering osteomalacia. The beneficial effect of this vitamin on Ca and P
metabolism continued for at least 4 months after administration of the vitamin had ceased. Liu et al. (1940) noted
that vitamin D supplementation rapidly improved Ca and P retention only when there was no reserve of the vitamin
in the body. McCance & Widdowson (1942a,b) and Hoff-Jorgensen et al. (1946a,b) found that supplementing a
diet containing phytate with vitamin D 2 did not increase Ca absorption. On the other hand, some workers
consistently showed in rats and chicks that dietary vitamin D markedly increased the utilization of phytin-P
(Krieger & Steenbock 1940, Boutwell et al. 1946, Spitzer et al. 1948, Steenbock et al. 1953). Mellanby (1949)
also reported that vitamin D lowered the amount of phytate P in the feces of dogs. Sommerville et al. (1985)
found that lowering dietary P markedly increased plasma 1,25(OH) 2D 3 in the chick, which was further increas ed by
increasing the level of dietary cholecalci ferol. Edwards (1993) reported dietary 1,25(OH) 2D 3 supplementation
increas ed phytate-P utilization in chickens.
McCay et al. (1927) fed brook trout fry for 12 weeks. The growth and mortality of the fish fed a
casein-starch diet supplemented with vitamin A and D (as cod liver oil) did not differ from those fed the same diet
but without the supplemental vitamins. Phillips et al. (1952) fed brook trout (initial wt. 0.94 g, wt gain ca.1200%)
for 20 weeks with a practical-type diet, and did not find any effects of dietary vitamin D3 supplementation on the
growth, feed efficiency, and proximate body composition. Phillips et al. (1955) also failed to see any positive
effects of vitamin D on growth, feed efficiency, and mortality in brook trout (initial wt. 1.4 g, final wt. ca.10 g).
This time, fish were fed for 20 wks with Wolf's synthetic diet (less cod liver oil) supplemented with corn oil with or
without the vitamin. Phillips et al. (1959) did not see any noticeable effects of dietary vitamin D2 in brook trout
on the assimilation of 32 P administered in one meal. However, Lovell & Li (1978) demonstrated that vitamin D is
an essential nutrient for growth and bone calci fi cation in channel catfish fingerlings. The responses reached a
plateau at 500 IU/kg diet. When a casein-based semi-purifi ed diet low in Ca (0.05%) but adequate in P was
supplemented with the vitamin, fish growth and the bone mineral contents (ash, P, Ca) increased markedly. With
adequat e amounts of vitamin D in diet, dietary Ca was apparently unnecessary (water contained 14 ppm Ca).
When a diet low in P (0.18%) but adequate in Ca was supplemented with the vitamin, fish growth and the bone
mineral contents did not increase. Barnett et al. (1982a) noted that a casein-based semi-puri fied diet free of
vitamin D3 did not alter Ca, P, AP, and Mg levels in plasma, and Ca and P levels in the bone of rainbow trout after
168 days of feeding. However, the fish growth differed markedly, which correl ated to the amount of vitamin D
added to the diet. Vitamin D3 was found to be more potent than vitamin D2. The feed conversion ratio and body
fat content decreased as the dietary level of vitamin D increased. There was a dose-dependent occurence of tetany
(up to 56%) among fish fed diets low in the vitamin. Barnett et al. (1982b) confirmed previous observations.
Fish fed a vitamin D free diet for 280 days had poor growth (47%) compared with growth of fish fed a diet
containing vitamin D3 in the amount of 1600 IU/kg. The fish in the vitamin deficient group had a higher incidence
of tetany (88%) than fish fed vitamin D-supplemented diet (13%). No fish showed vertebral abnorm ality, and
apparently no motality was recorded associat ed with tetany. The vitamin deficient fish showed muscle weakness,
but they were neither hypocalcimic nor hyperphosphat emic. The authors therefore suggested that the functions of
vitamin D in trout appeared to be quite different from those in terrestrial animals.
Avila et al. (1999) fed rainbow trout (body wt. 56 g) for 7 or 8 days with P-suffici ent diets (0.6%P) differing
in VD 3 content (0, 300, 2,500, 10,000, 40,000 IU/kg). Plasma Pi was slightly higher (8.3 vs 7.0 mmol/L) in fish
fed diets containing 2,500-40,000 IU VD3/kg than those fed diets containing 0 or 300 IU VD3/kg. However,
plasma levels of 25(OH)D 3 and 1,25(OH) 2D 3 did not differ. Increasing the level of dietary VD3 also did not
increas e an in vitro Pi uptake from the intestine. Also, the iIn vitro Pi uptake did not differ among tissues
pre-incubated in a solution containing VD 3, 25(OH)D 3, 1,25(OH) 2D 3, or Ringer (placebo). Ashok et al. (1999) fed
© 2000, 2005. Shozo H. Sugiura. All rights reserved.
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