Review: Phosphorus in Fish Nutrition

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ats, Meyer et al. (1992) and Sriussadaporn et al. (1995) found that low dietary P up-regulates intestinal VDR mRNA abundance in the intestine. The increased gene expression, however, was modest in magnitude, brief in duration and limited only to intestinal tissues. Fish VDR mRNA sequences have been identified in zebrafish and flounder; however, the functional roles have not been studied. In flounder, VDR mRNA appears to be omnipresent, but it may be absent in liver (Suzuki et al. 2000). In chickens, however, a trace amount of VDR mRNA was present in liver (Lu et al. 1997). In trout, VDR mRNA appears to be distributed in various tissues. In trout, intestinal VDR mRNA abundance was apparently independent of diet at all times, while renal VDR mRNA increas ed significantly at d5 (~2 fold) but not at d2 or d20 of dietary P restriction. Segawa et al. (2004), however, reported that VDR-null mice increased intestinal NaPi mRNA and protein expressions as well as Pi transport in dietary P restriction, suggesting that intestinal NaPi-II expression is also mediated via a mechanism that is independent of the vitamin D-signaling. Phosphatonins are hypophosphatemic factors that cause phosphaturia in mammals, which include fibroblast growth factor 23 (FGF23), frizzled related protein 4 (FRP4), and matrix extracellular phosphoglycoprotein (MEPE). FGF23 is highly expressed in certain tumors (tumor-induced osteomalacia: TIO) and in FGF23 gene mutations (ADHR) (Takeda et al. 2000). FGF23 may be the (indirect) substrate for PHEX that is expressed in hard tissues. Thus, in patients of X-linked hypophosphatemia (XLH), who have a PHEX gene mutation, FGF23 accumulates in circulation, causing renal P wasting. In mammals, patients of chronic renal failure (accompanied by hyperphosphatemia) show elevated circulating FGF23. FGF23 suppresses CYP27B1 expression in kidney, and both NaPi-IIa and IIb expression, causing reduction of Pi absorption in both kidney and intestine. 1,25(OH) 2D3 injection increases serum Pi and FGF23. Serum Pi and FGF23 concentrations appear to be highly and positively correlated one another. There is presently no sequence in fish EST databases that shows significant homology to mammalian FGF23. Thus, the roles of FGF23 in fish remain to be studied. Custer et al. (1997) found another gene that was up-regulated by ~2 fold in dietary P restriction, which they tentatively called diphor-1 (currently PDZK1). PDZK1 and other PDZ proteins such as NHERF1 appear to participate in the apical-cytosolic traffi cking of NaPi-IIa protein in mammals (Biber et al. 2004). PiUS is an inositol hyxakisphosphate (IP6) kinase, which transfers Pi from diphosphoinositol pentakisphosphate (PP-IP5) to ADP to form ATP. Norbis et al. (1997) identified a cRNA in rabbit small intestine that stimulates Pi uptake when injected into Xenopus oocytes, which they tentatively called inorganic phosphate (Pi)-uptake stimulator or PiUS. Subsequently, PiUS mRNA was found to be upregulated about two folds in rat intestine after 7 days of dietary P restriction (Katai et al. 1999). In trout, however, PiUS mRNA in the intestine and kidney appears to be insensitive to dietary P restriction. Mitochondrial Pi carrier protein appears to be up-regulated (~3-fold) in dietary P-restriction in rainbow trout. This protein transfers Pi from cytosol to mitochondrial matrix for oxidative phosphorylation. Thus, up-regulating (increasing) this protein might be necessary to supply Pi to the respiratory chain under limited cytosolic Pi concentrations. In mammals, acute hypophophatemia, typically associated with glucose perfusion, causes the so called Crabtree effect that reduces ATP production due to competition between glycolysis and oxidative phosphorylation under limited cellular Pi availability (Brazy & Mandel 1986, Brazy & Chobanian 1996). Chronic hypophosphatemia is also known to be associated with decreas ed erythrocyte ATP concentration in animal species (Knochel 1977). In trout, however, blood ATP concentration seems to decreas e only slightly and muscle ATP changes little by chronic (24 d) dietary P restriction, which might be due to the up-regulation of mitochondrial Pi carrier protein. Kuro-o et al. (1997) found a single gene that is associated with several aging-related syndromes. They named the gene klotho gene. Klotho (Clotho) is a Greek goddess who spins the thread of human life. The length of the string will determine how long a certain person's life will be. Klotho gene is expressed predominantly in kidney and brain. Interestingly, Yoshida et al. (2002) found, in klotho -/- mice, that serum 1,25(OH) 2D was markedly elevat ed; renal CYP27B1 mRNA was also markedly upregulated; renal CYP24 mRNA was slightly upregulated, serum P and Ca were also elevated; serum CT was slightly elevated; and serum PTH was slightly decreased compared with wild-type mice. Morishita et al. (2001) found in klotho mutant mice that low-P diet prevented the progression of senes cence, and even induced the expression of klotho protein. Also, in wild-type mice, high-P diet decreased renal klotho protein expression. Fish have no parathyroid gland; however, Gensure et al. (2004) has identified, in zebrafish and pufferfish, PTH/PTHrp (parathyroid hormone-related peptide) receptors. These investigators also identified two different PTH in zebrafish that bind to these receptors. The PTH genes are reported to be expressed in the lareral line (embryo, transient) and in the brain and neural tissues (only PTH1). The physiological roles of fish PTH, however, remain to be studied. Calcitonin (CT) is a hypocalcimic hormone in mammals, which also appears to affect P homeostasis. CT decreases blood Ca level by decreasing Ca absorption in the intestines, by decreasing Ca © 2000, 2005. Shozo H. Sugiura. All rights reserved. 14
eabsorption in the kidney, and by decreasing osteoclast activity. In fish CT is secreted from the ultimobrachial glands, but the role is not well-defined. Wagner et al. (1997) reported that salmon CT inhibited gill Ca uptake in trout. Stanniocalcin (STC) prevents hypercalcemia in fish by inhibiting gill Ca uptake. STC also stimulates renal Pi reabsorption in fish (Lu et al. 1994). Lu et al (1994, 1995) reported a wide variety of factors regulating P metabolism in fish using flounder renal tubule cell cultures, where net Pi reabsorption was increased by salmon stanniocalcin, rat prolactin, salmon/flounder somatolactin, bovine PTH (bovine), and salmon growth hormone. In mammals, STC decreases net Ca transport and increas es net Pi transport in the intestine, increases Pi reabsorption in kidney, and increases Pi uptake in osteogenic cells (via type-3 NaPi). Mammalian STC appears to have many other functions (Ishibashi & Imai 2002, Yoshiko & Aubin 2004). In rats, Cheung et al. (2002) reported six P responsive genes, including beta-actin, in the renal proximal tubules based on proteomics. Indicators of P status: Perspectives Some molecular indicators appear to be more sensitive and reliable than traditional indicators to diagnose body P status and to predict potential dietary P deficiency. However, as discussed above, molecular indicators are relatively difficult to analyze, making their practical use limited. But, do we need to analyze anything? In the near future, P status of fish may be “ expressed” by the fish by way of their body color, for eample. A recent study on plant P-responsive genes suggests that P responsive genes may be modified (Hammond et al. 2003, 2004). Such genes may contain a P-response element, such as vitamin D response element, in the promoter region upstream of the transcription initiation site. Then, the P-responsive promoter is fused to a reporter gene, such as melanin (instead of luci ferase), and inject it back into the original fish (embryo). The expression of such genes may be tissue or cell specific. Where the cell type is appropriate, the fused marker gene will be turned on when dietary P intake is inadequate, increasing the transcription of melanin mRNA, making the fish darker in color. Such marker fish may eventually replace all laboratory analysis. It will be necessary, however, to identify the P responsive gene in the skin, unless P-responsive gene from other tissues can be adequat ely expressed in the skin. Also, the mRNA to protein translation may be regulated. When fish look dark in color, simply increase dietary P a little, and when they look normal, try reducing dietary P until some of them become dark. A fine adjustment of dietary P concentration can be done by using two diets, one slightly P-defi cient and another slightly P-excess, and mixing them at an optimum ratio based on the fish color. This will be particularly useful since, as mentioned above, dietary P requirement varies greatly depending on many factors, including feed quality, developmental or physiological stage, and cultural conditions. P requirement for large or adult fish First of all, we should consider the reasons why there is no data on large fish. The most important reason is that large fish are quite resistant to nutrient deficiency compared with small fish, and thus they do not respond to dietary restriction of nutrients if conventional response indicators are used. My calculation (based on body P reserve and shifting feed effi ciency during the life stages) indicates that when small fish (1g body weight) are fed P-deficient diet containing 0.2% available P, their growth will be arrested in seven days on the diet. For fish of 10 g body weight, it takes 20 days before their growth is depressed. For fish of 500 g body weight, it takes 232 days of feeding, and for fish of 1 kg, their growth will never respond to the diet. Major factors responsible to these differences are that: (1) large fish may have large initial body P store, (2) large fish have lower feed efficiency than small fish, and (3) large fish have lower feeding rate per body weight. Therefore, it is probably impossible to accurately determine dietary P requirement for large fish based on growth rate. This does not mean that large fish can be reared on P-deficient feeds because their initial P store is not known. Thus, it is important to know the P requirem ent for large fish to minimize the risk of P-depletion (see section “Phase-feeding and finishing feed”). Satoh et al. (1987) wrote, "Fish weighing over 2 g are not suitable as experimental animals for determination of mineral requirements in terms of diffi culty to induce mineral defici ency." This is probably true; however, it is still necessary to know the nutrient requirements of large fish regardless of the diffi culty, as Cowey (1995) states, "Since about 90% of the food used in fish farming is given to large fish (100 g
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Page 3 and 4: maximizing the bone strength, blood
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Page 9 and 10: tubular secretion (as in birds and
Page 11 and 12: Knochel 2000; Haglin 2001). These c
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Page 31 and 32: freshwater fish Labeo rohita (Rora)
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Page 35 and 36: NaCl 1%, and CaCO 3 3%. The Ca/P ra
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Page 41 and 42: increas e urinary P. Boling et al.
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Page 49 and 50: P contents in the whole body and ve
Page 51 and 52: Barros, F. -- J. de Chim. med. T.4,
Page 53 and 54: Cromwell, G.L., Coffey, R.D., Parke
Page 55 and 56: (Sciaenops ocellatus). Aquaculture,
Page 57 and 58: Forbes & Keith 1914, pp. 436) Higur
Page 59 and 60: Kempson, S.A., Kim, J.K., Northrup,
Page 61 and 62: hypophosphatemia. Ann. Int. Med. 74
Page 63 and 64: Mellanby, E. 1924. Deficiency disea
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Ogino, C., Takeda, H., 1976. Minera
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Radunz-Neto, J., Corraze, G., Charl
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different dietary calcium levels on
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Sugiura, S.H., Dong, F.M., Rathbone
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eproduction of red sea bream. Bull.
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Table 1. Availability of Phosphoru
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(1982), 6 Watanabe et al. (1980a),
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Ash, Ca, P (muscle) 21, 31, 35, P,
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Table 3. Reference Values for Diagn
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(Vielma & Lall 1998a; 40 g), 4 (Ogi
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Figure 1. Ventral view of P-defi ci
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Figure 6. Pyloric caeca are the maj
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Review: Phosphorus in Fish Nutrition

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