Page 127 - Small Animal Clinical Nutrition 5th Edition
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128        Small Animal Clinical Nutrition



                  Vitamin D                                           vitamin D status.
        VetBooks.ir  Two important forms of vitamin D are cholecalciferol (vitamin  tem: 1,25-(OH) -D , PTH, calcitonin, several other hor-
                                                                        Several factors tightly regulate the vitamin D endocrine sys-
                  D ), which occurs in animals and ergocalciferol (vitamin D ),
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                                                                      mones and circulating levels of calcium and phosphate. The
                  which occurs predominantly in plants. In pet food, vitamin D
                  activity is typically expressed in IU. One IU of vitamin D can  vitamin D-dependent homeostatic system responds to pertur-
                  be provided by 0.025 µg of cholecalciferol or vitamin D . The  bations in calcium concentration. For example, when serum
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                  skin of most mammals can produce cholecalciferol from the  calcium falls below a given level, PTH is secreted by the
                  provitamin 7-dehydrocholesterol via activation with ultraviolet-  parathyroid glands, which function to detect hypocalcemia.
                  B light. However, this photosynthesis pathway is inefficient in  The kidney responds to PTH, resulting in phosphate diuresis
                  dogs (Hazewinkel et al, 1987) and cats (Morris, 1999) because  and stimulation of 25-OH-D 1-hydroxylase.The latter effect
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                  of the higher activity of the enzyme 7-dehydrocholesterol- ∆ 7  increases production of 1,25-(OH) -D , which acts to
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                  reductase that converts 7-dehydrocholesterol to cholesterol.  increase enteric absorption of calcium and phosphate. In addi-
                  Therefore, dogs and cats need dietary vitamin D.    tion, 1,25-(OH) -D acts jointly with PTH in bone to pro-
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                                                                      mote mobilization of calcium and phosphate. The combined
                    FUNCTION                                          result of these responses is to increase plasma concentration of
                    The primary function of vitamin D is to enhance intestin-  calcium and phosphate. Calcitonin is secreted by the thyroid
                  al absorption and mobilization, as well as retention and bone  gland (“C” cells) when circulating concentrations of calcium
                  deposition of calcium and phosphorus. This function is man-  are increased. Calcitonin suppresses bone mobilization and
                  ifested through its active form of 1,25-(OH) -D as a hor-  may increase the renal excretion of calcium and phosphate. In
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                  mone that binds to the nuclear 1,25-(OH) -D receptor  that situation, 25-OH-D 1-hydroxylase may be inhibited by
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                  (VDR) in many types of cells. The active vitamin D also has  1,25-(OH) -D , and may actually be converted to 24,25-
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                  a direct effect on Ca 2+  channels located on the plasma mem-  (OH) -D , which may down-regulate the absorption of calci-
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                  brane (Norman et al, 1992).                         um in dogs (Tryfonidou et al, 2002).
                                                                        These events tightly regulate hydroxylase activity and main-
                    METABOLISM                                        tain nearly constant plasma concentrations of 1,25-(OH) -D ,
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                    Vitamin D is absorbed from the small intestine by nonsat-  calcium and phosphorus. Once formed, 1,25-(OH) -D binds
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                  urable, passive diffusion, which depends on bile salts. Vitamin  to specific receptors on the enterocyte nucleus and initiates
                  D then enters the lymphatic circulation primarily (~90%) in  events that stimulate calcium and phosphorus absorption. In
                  association with chylomicrons; the remainder of vitamin D is  addition, 1,25-(OH) -D , acting with PTH, mediates resorp-
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                  associated with an  α-globulin fraction (Combs, 1998). Like  tion of bone with the release of calcium and phosphorus.
                  other steroids, vitamin D is transported in association with pro-  Many metabolites of vitamin D circulate in plasma other
                  teins. In most species, the binding protein is vitamin D-bind-  than 25-OH-D 3  and 1,25-(OH) -D . One metabolite,
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                  ing protein (DBP) or “transcalciferin.” The concentration of  24,25-(OH) -D , may also be biologically active, whereas
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                  DBP greatly exceeds the concentration of vitamin D metabo-  other metabolites are generally considered physiologically inac-
                  lites in blood. This concentration difference, in conjunction  tive excretory forms (Combs, 1998).
                  with the binding affinity, results in less than 5% of the available
                  binding sites being occupied by vitamin D compounds. The  REQUIREMENTS
                  distribution between bound and free vitamin D compounds  The AAFCO (2007) dietary allowance for vitamin D is 500
                  greatly favors the bound form. In this fashion, DBP facilitates  IU/kg DM for dogs for all lifestages. For cats, the AAFCO
                  peripheral distribution of vitamin D from dietary origin and  (2007) allowance is 750 IU/kg DM for growth and reproduc-
                  mobilizes endogenously produced vitamin D from the skin.  tion and 500 IU/kg DM for maintenance. The vitamin D
                    Vitamin D is distributed relatively evenly among the various  allowance recommended by NRC (2006) is 13.8 µg cholecal-
                  tissues where it resides in lipid depots. Vitamin D can be found  ciferol (552 IU)/kg DM for dogs regardless of lifestage. The
                  in adipose, kidneys, liver, lungs, aorta and heart. The primary  NRC recommended vitamin D allowance for cats is 5.6 µg
                  circulating form of vitamin D is the parent vitamin D (~50%),  cholecalciferol (250 IU)/kg DM for growth and 7 µg cholecal-
                  with the next most abundant form (i.e.,25-OH-D [also called  ciferol (280 IU)/kg DM for maintenance and reproduction.
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                  calcidiol]) accounting for approximately 20% of the total
                  (Combs, 1998).                                        DEFICIENCY AND TOXICITY
                    In mammals, both vitamin D and D are not the active  Signs of vitamin D deficiency are frequently confounded by
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                  form of vitamin D. They are activated in the body by hydrox-  a simultaneous deficiency or imbalance of calcium and phos-
                  ylation to 25-OH-D first in the liver and again to 1,25-  phorus. Clinical signs generally include rickets (young ani-
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                  (OH) -D (also called calcitriol) in the kidneys. Vitamin D 2  mals), enlarged costochondral junctions, osteomalacia (adult
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                  is less efficiently used than vitamin D in cats (Morris, 2002).  animals), osteoporosis (adult animals) and decreased serum cal-
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                  At normal plasma concentrations, only small amounts of 25-  cium and inorganic phosphorus concentrations. Experimental
                  OH-D are released from this pool to enter tissues.Thus, cir-  vitamin D deficiency has been produced in cats, resulting in
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                  culating levels of 1,25-(OH) -D are a good indicator of  neurologic abnormalities associated with degeneration of the
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