vitamin d deficiency in animals

Vitamin D benefits the body by playing a role in immunity and controlling cell growth. Although vitamin D is critical to calcium/phosphorus homeostasis, bone formation and remodeling, there is evolution-based variation between species in vitamin D metabolism and susceptibility to rickets and osteomalacia. The dogma that mammals (other than the New World monkey) do not discriminate between vitamin D2 and D3 has proven incorrect. There are small amounts of vitamin D in some foods such as fish, eggs and UV-irradiated mushrooms, but it is difficult to obtain enough vitamin D from diet alone. The discovery and synthesis of the nutritional factor vitamin D. [Brief history of rickets and of the discovery of vitamin D]. The therapeutic value of vitamin D and its analogs has been under rigorous evaluation in numerous laboratories around the world. The mechanism whereby vitamin D stimulates calcium and phosphorus absorption is still not completely understood. The dog showed no lameness but was lethargic and inactive. Hormone Research. The darker the skin the longer time required to convert 7-dehydrocholesterol to vitamin D3.Presence of the provitamin 7-dehydrocholesterol in the epidermis of the skin and sebaceous secretions is well recognized. The differential utilization between cholecalciferol (vitamin D3) and ergocalciferol (vitamin D2) has not been investigated in dogs, but in cats cholecalciferol is utilized more efficiently than is ergocalciferol to maintain plasma concentrations of 25-(OH)D (Morris, 2002). Studies in a number of species indicate that vitamin D3 is 10 to 20 times more toxic than vitamin D2 when provided in excessive amounts (NRC, 1987). Three were dead within two weeks and a fourth was moribund in five weeks. Vitamin E-AD Injectable d-alpha-tocopherol with AD is a clear, sterile water emulsifiable solution of vitamin A, vitamin D 3, and vitamin E. This product is intended for use as an aid in the prevention and treatment of vitamin E deficiencies in swine, cattle and sheep. For grazing livestock in the presence of UV light, no dietary sources of vitamin D are required. Vitamin D deficiency in dogs and cats receiving commercially prepared foods is not common. To date, more than 50 genes have been reported to be transcriptionally regulated by 1,25-(OH)2D (Hannah and Norman, 1994).Vitamin D has also been shown to be required for embryonic development of the chick. In 1922, Mellanby of Great Britain produced rickets in dogs by feeding them oatmeal (McDowell, 2000). Its potency depends on local climatic conditions. : Solanum spp., Cestrum diurnum, and Trisetum flavescens) containing various forms of vitamin D including vitamin D 2 and 1,25-dihydroxycholecalciferol-glycoside, excess dietary supplementation, or ingestion of rodenticides containing cholecalciferal (vitamin D3) (Craig et al., 2016; Crossley et al., 2017). Dogs with rickets became lethargic and had a general loss of muscular tone which did not allow them to run quickly. Int Orthop. Feeding a milk replacer to airedale puppies resulted in poor development and condition, impaired moving capacity, retarded change of teeth and pathological changes in the kidney (renal calcification and sclerosis, fibrosis of glomerula, dilation of the tubuli). Rapid, acute plasma calcium regulation is due to the interaction of plasma calcium with calcium-binding sites in bone material as blood comes in contact with bone. However, when the diet contained 0.08% to 0.10% calcium and 0.13% to 0.15% phosphorus and no supplemental vitamin D, rickets complicated by osteoporosis was observed. Vitamin D: part II; cod liver oil, ultraviolet radiation, and eradication of rickets. Epub 2010 Jul 15. Sources of vitamin D are feedstuffs, irradiation, sebaceous material licked from skin or hair or directly absorbed products. The third important variable determining skin vitamin D synthesis is the actual concentration of 7-dehydrocholesterol present in the skin. Please enable it to take advantage of the complete set of features! It may be supplied through the diet or by irradiation of the body. It most commonly occurs in people when they have inadequate sunlight exposure (in particular sunlight with adequate ultraviolet B rays (UVB)). doi: 10.1016/j.heliyon.2019.e01432. Under normal conditions, even wilting legume silage furnishes ample vitamin D for livestock. It is generally characterized by a decreased concentration of calcium and phosphorus in the organic matrices of cartilage and bone. This function is shared by PTH (Garabedian et al., 1974), requires metabolic energy, and presumably transports calcium and phosphorus across the bone membrane by acting on osteocytes and osteoclasts. After two months, the gastrointestinal and skin disorders disappeared, although calcification of the stomach membranes remained and abnormality of the skeletal system had worsened. (2003) reported both 25-(OH)D3 and 1,25-(OH)2D3 to be significantly lower in dogs with acute renal failure and chronic renal failure. Metabolites. Vitamin D deficiency is associated with a range of clinical disorders. Rickets is more common with diets that are low in vitamin D and have an accompanying deficiency in dietary calcium and/or phosphorus, or with diets that are imbalanced with respect to calcium and phosphorus (where calcium percentage is less than phosphorus). Vitamin K is a fat-soluble vitamin essential for the post-translational processing of the prothrombin group of coagulation factors (Factors II, VII, IX, and X). By itself vitamin D is biologically inactive and must be converted to a hormonal form in a two-step process before it can function as the hormone 1,25-(OH)2D3. In young animals Vitamin D deficiency causes true "rickets" which is a disorder of bone and cartilage due to poor mineralisation with calcium and phosphorus. Commonly, problems related to sex bug men due to the general perspective that they seem to be ones in control of the entirety of a sexual activity. Copyright © 2018 The Author. Caution for vitamin D toxicity must also be used when formulating home diets for dogs and cats or when enhancing the palatability of commercial diets with higher levels of liver or fish oil, which are all rich sources of vitamin D. Strombeck (1999) hypothesizes that the high incidence of kidney disease in dogs and cats may be related to commercial pet foods that contain excess vitamin D. This site uses cookies to store information on your computer. Chronic renal disease interferes with the production of 1,25-(OH)2D3 by the kidney, thereby diminishing intestinal calcium transport and resulting in development of hypocalcemia. Data for the pig (Horst and Napoli, 1981) and for ruminants (Sommerfeldt et al., 1981) suggest that these species discriminate in the metabolism of vitamin D2 and D3, with the vitamin D3 being the preferred substrate. 65,106 Affected individuals have normal serum 25(OH)D 3 concentrations and low 1,25(OH) 2 D 3 concentrations. They may also be lethargic, have depressed appetites, and may walkwith a hunched back due to pain and are typically smaller than age-matched herdmates. Vitamin D and food. Clinical signs of bleeding depend on duration and severity of vitamin K deficiency and include prolonged bleeding from minor wounds, spontaneous hematoma formation, intracavitary hemorrh… Vitamin D deficiency, or hypovitaminosis D is defined as a vitamin D level that is below normal. It is a good point - polar animals probably get their Vitamin D levels from eating fish. The receptor-hormone complex moves to the nucleus where it binds to the chromatin and stimulates the transcription of particular genes to produce specific mRNAs, which code for the synthesis of specific proteins. Tryfonidou et al. Michaud and Elvehjem (1944) concluded that, with a dietary calcium:phosphorus ratio of 1.2:1, daily intakes of 10 to 20 IU vitamin D per kg (4.5 to 9.1 IU per lb) of body weight were adequate, even for large breeds.The current NRC (2006) vitamin D recommendations for dogs is 13.8 µg of vitamin D3 per kg of diet (6.3 µg per lb) for all classes of dogs. (1983) reported that the amount of 1,25-(OH)2D in the plasma of ergocalciferol-treated dairy calves was one-half to one-fourth the amount of the cholecalciferol-treated calves. Vitamin D Deficiency in Dogs Known as the “sunshine vitamin” because exposure to sunlight helps the body produce it naturally, vitamin D is an essential vitamin for dogs, which means the dog’s own body does not produce a sufficient amount and therefore vitamin D must be included in the animal’s diet for the dog to maintain optimal health. Young animal especially need adequate amounts of vitamin D to develop strong bones. Cholecalciferol (vitamin D3) rodenticides have caused significant toxicity in dogs at a fraction of the manufacturer’s reported LD50 for dogs, 88 mg pure cholecalciferol per kg (40 mg per lb) (Garlock et al., 1991). 1,658 adults aged 65 and over were included in the study and followed over a period of six years.. There is less destruction of vitamin D3in freeze-dried fish meals during drying, possibly because of decreased atmospheric oxygen. An animal’s diet affects the amount of vitamin D in its tissues. Acta Reumatol Port. Zafalon RVA, Ruberti B, Rentas MF, Amaral AR, Vendramini THA, Chacar FC, Kogika MM, Brunetto MA. Your GP may recommend taking a vitamin D supplement. Keywords: doi: 10.1530/EC-20-0274. Stabilization of the vitamin can be achieved by (a) rapid compression of the mixed feed, for example, into pellets so that air is excluded; (b) storing feed under cool, dry, dark conditions; (c) preventing close contact between the vitamin and potent metallic oxidation catalysts (e.g., manganese); (d) including natural or synthetic antioxidants in the mix. With a few notable exceptions, vitamin D3, is not found in plants. This stimulation does not involve PTH directly but involves the active form of vitamin D. Parathyroid hormone indirectly stimulates intestinal calcium absorption by stimulating production of 1,25-(OH)2D3under conditions of hypocalcemia. In the dogs that survived, malocclusion, pitting, irregular placement, and poor development of the teeth were seen.Hendricks et al. Kozelka et al. Effects of overdosage of vitamin D were observed at necropsy in a cat that had been given 5 million IU of vitamin D3and 2.5 million IU of vitamin A by mouth over a six-month period. Deficiency of Vitamin D has been linked to certain types of cancers including cancers of the breast, colon, and prostate including several other chronic health conditions. Recent studies have suggested 1,25-(OH)2D3 as an immunoregulatory hormone. Parenteral cholecalciferol treatment of sows before parturition proved an effective means of supplementing young piglets with cholecalciferol (via the sow’s milk) and its more polar metabolites via placental transport (Goff et al., 1984). The current dietary vitamin D recommendation of theNRC (2006) for kittens is that they be provided 5.6 µg vitamin D3 per kg (2.5 µg vitamin D3 per lb) of diet. This site needs JavaScript to work properly. In response to the 1,25-(OH)2D, specific RNAs are elaborated by the nucleus, and when these are translated into specific proteins by ribosomes, the events leading to enhancement of calcium and phosphorus absorption occur (Scott et al., 1982).In the intestine, 1,25-(OH)2D3 promotes synthesis of calbindin (calcium-binding protein, CaBP) and other proteins and stimulates calcium and phosphorus absorption. NIH (1957b) found that 250 IU of cholecalciferol given orally, twice a week, prevented the development of rickets in kittens fed a semi-purified diet from three to six months of age to 21 months of age. Deficiency. During the winter time there islittle possibility of vitamin D production … The supplement contained excess vitamin D at 3.45 million IU per kg (1.57 million IU per lb). Vitamin A is an essential canine vitamin. To study the mechanisms involved and improve treatments, animal models are tremendously useful. Int J Paleopathol. 2020 Dec 3;10(12):496. doi: 10.3390/metabo10120496. The incomplete calcification of the skeleton is easily detectable with X-rays and reduced bone ash but, like other production-related signs, would not be specific for vitamin D deficiency versus other nutrient inadequacies (e.g., calcium and phosphorus). The two receptors (vitamins D and A) selectively interact with specific hormone response elements composed of direct repeats of specific nucleotides located in the promoter of regulated genes. 2018 Dec;23:96-99. doi: 10.1016/j.ijpp.2018.01.002. However, this question was probably answered in a study where the 24-position of 25-(OH)D3 was blocked with fluoro groups to prevent 24-hydroxylation (DeLuca, 2008). On a feed basis, AAFO (2007) recommends 750 IU per kg (341 IU per lb) for cats in growth and reproduction and 500 IU per kg (227 IU per lb) for maintenance. (1998) reported that vitamin D deficiency depresses the cellular immune responses in young broiler chicks. Most herbivores produce vitamin D 3 in response to sunlight, but dogs and cats have generally lost the ability as carnivore diets are rich in vitamin D. Nutritional deficiencies and/or poor exposure to sunlight can induce rickets in birds, swine, cattle and sheep, but horses are less susceptible as they have evolved a calcium homeostasis that is quite different than other animals. Because toxic manifestations of hypervitaminosis D are associated with hypercalcemia, serum calcium levels must be closely monitored when 1,25-(OH)2D3 is given (Lewis et al., 1987; NRC, 2006). Also, 1,25-(OH)2D3 and its analogs may be effective in treating some forms of psoriasis (Kragballe et al., 1991). Animal Physiology. For concentrate feed mixtures, the vitamin D that occurs naturally in unfortified feed is generally derived from animal products. A deficiency of vitamin D may promote prostate cancer (Skowronski et al., 1995). Vitamin D metabolism and rickets in domestic animals: a review. 1,25-(OH)2D3 regulates gene expression through its binding to tissue-specific receptors and subsequent interaction between the bound receptor and the DNA (Norman and Henry, 2006). symptoms of vitamin d deficiency in animals. In the adult, osteomalacia is the counterpart of rickets and, since cartilage growth has ceased, is characterized by a decreased concentration of calcium and phosphorus in the bone matrix. During times of deprivation, vitamin D in these tissues is released slowly, thus meeting vitamin D needs of the animal over a longer period of time (Norman and Henry, 2007). There is negligible loss of crystalline cholecalciferol during storage for one year or of crystalline ergocalciferol for nine months in amber-evacuated capsules at refrigerator temperatures.Vitamin D from the diet is absorbed from the intestinal tract, and is more likely to be absorbed from the ileal portion in greatest amounts due to the longer retention time of food in the distal portion of the intestine (Norman and Henry, 2007). Rickets/osteomalacia were likely more common in animals before the advent of commercial diets, but can be difficult to definitively diagnose especially in single archeological specimens. In dogs with chronic renal disease, 1,25-(OH)2D3 has been advocated for use as a therapeutic agent in the prevention of hypocalcemia and osteodystrophy, with daily dosages as high as 0.1 µg per kg (0.05 µg per lb) body weight (Lewis et al., 1987). Production and metabolism of vitamin D necessary to activate the target organs is illustrated in Figure 3-1. More advanced cases interfere with cartilage growth. It is commonly seen in cattle and sheep in feedlots, and also those being fed high concentrate diets in the absence of green pasture, as is common during droughts. Species differences can be illustrated by the fact that adequate intakes of calcium and phosphorus in a diet that contains only enough vitamin D to produce normal bone in the rat or pig will quickly cause the development of rickets in chicks. Over-supplementation of vitamin D was a risk factor for chronic heart failure in fast growing commercial broilers (Nain et al., 2007). Although there appear to be differences among species in the susceptibility of different bones to such degenerative changes, as well as differences that probably reflect bodily conformation (e.g., dog compared with sheep), there is nevertheless an apparent common pattern (Abrams, 1978). Mellanby (1921), in a summary of his studies on rickets (in which nearly 400 puppies were used), stated that rickets occurred more rapidly in fast-growing than slow-growing dogs. (1991), in studies with weanling pups, suggested that supplementation of nonpurified, commercially available dog foods with vitamin D may not be necessary. Next come the scapula, sternum and ribs. The Role of Vitamin D in Small Animal Bone Metabolism. In particular, vitamin A and E can be common causes of lost profit, secondary to limitations of reproductive and growth potential. The remaining 1% is under control of these two hormonal agents, although it is not known whether they work in concert. Vitamin D Metabolism and Profiling in Veterinary Species. Vitamin D is made in the skin by the action ofUV light: it can also be consumed in the diet. The cats that died during acute rickets had a lower percent femur ash than did cats supplemented with vitamin D. Experimental vitamin D deficiency has been produced in cats, resulting in neurologic abnormalities associated with degeneration of the cervical spinal cord (Morris. Boosting Female Libido. This is because the dead or injured leaves on the growing plant are responsive to UV irradiation even though the living tissues are not. The number of calbindin neurons decreased in the aged dog brain and this may be associated with reduction of function in the dentate gyrus. Rickets in dogs is similar radiographically, histopathologically, and biochemically to the disease in other animals or human beings. Changes in plasma calcium are brought about by a change in the proportion of high- and low-affinity calcium-binding sites, access to which is regulated by osteoclasts and osteoblasts, respectively (Bronner and Stein, 1995). Kittens from queens receiving a diet containing a high level of vitamin D (400 µg cholecalciferol per kg or 181.8 µg per lb) during pregnancy and lactation were able to complete their growth phase without clinical signs of vitamin D deficiency. Stability of dry vitamin D supplements is affected most by high temperature, high moisture content and contact with trace minerals such as ferrous sulfate, manganese oxide and others. Morgan et al. Toxicosis due to the ingestion of these products must therefore be included in the differential diagnosis for hypercalcemia in dogs and cats. The symptoms are specific to each animal species. Vitamin D is an essential part of the nutrition for dogs as it helps in their muscle and bone development. The dog was one of the first animals in which rickets was produced experimentally. Alfalfa, for example, will range from 650 to 2,200 IU per kg (295 to 1,000 IU per lb) (Maynard et al., 1979). Grains, roots and oilseeds and their numerous by-products for livestock feeds contain insignificant amounts of vitamin D; green fodders are equally poor sources. Other signs included hypocalcemia, posterior paralysis, ataxia and eventual quadriparesis. Vitamin D Deficiency. This process causes bones to elongate. Vitamin D has also been reported to influence magnesium absorption as well as calcium and phosphorus balance (Miller et al., 1965). The principal source of the antirachitic factor in the diets of farm animals is provided in the action of radiant energy upon ergosterol in forages. Reports of hypervitaminosis D in cats have resulted from either accidental ingestion of rodenticides containing cholecalciferol as the active ingredient, consumption of diets based on fish (particularly fish viscera), or errors in diet formulation. This calbindin is not present in the intestine of rachitic chicks but appears following vitamin D supplementation. Why do so many trials of vitamin D supplementation fail? For dogs, a high dose of 1,25(OH)2D3 has been shown to exhibit antitumor activity for some animals and is used in cancer chemotherapy (Rassnick et al., 2011). Serum biochemical abnormalities were hypocalcemia, hypomagnesemia, and hyperparathyroidism. As would be expected, the skeletal system undergoes a simultaneous demineralization that results in the thinning of bones. After vitamin A, vitamin D is the vitamin next most likely to be consumed in concentrations toxic to animals. Vitamin D results in clinical signs similar to those indicating a lack of calcium or phosphorus or both, as all three are concerned with proper bone formation. Once in the liver, the first transformation occurs in which a microsomal system hydroxylates the 25-position carbon in the side chain to produce 25-hydroxy-vitamin D [25-(OH)D]. The actions of 1,25-(OH)2D are recognized as being involved in regulation of the growth and differentiation of a variety of cell types, including those of the hematopoietic and immune systems (Lemire, 1992). Rivers et al. Excretion of absorbed vitamin D and its metabolites occurs primarily in feces with the aid of bile salts. Endocrinology. The cat received these vitamins as treatment for a skin ailment, but gradually lost weight and died suddenly. By knowing what vitamin A does for your dog and what symptoms to look for, you can help protect your pet from this serious vitamin deficiency. The primary vitamin D deficiency disease is a bone disorder called rickets in young animals. Nutritional rickets: Historic overview and plan for worldwide eradication. Current evidence (Wasserman, 1981) indicates that 1,25-(OH)2D is transferred to the nucleus of the intestinal cell, where it interacts with the chromatin material. Like the others, it requires the presence of bile salts for absorption (Braun, 1986), and is absorbed with other neutral lipids via chylomicron into the lymphatic system of animals. For rickets in kittens, serum alkaline phosphatase activity increased markedly in the third month, peaked during the fifth to seventh months, and decreased through the twenty-first month. (2009) compared calbindin immunoreactivity in the dentate gyrus of dogs of various ages (German shepherds). COVID-19 is an emerging, rapidly evolving situation. Milk contains a variable amount in it’s fat fraction (5 to 40 IU in cow milk per quart), but neither cow nor human milk contains enough to protect the newborn against rickets (Maynard et al., 1979). Diffuse calcification affects joints, synovial membranes, kidneys, myocardium, pulmonary alveoli, parathyroids, pancreas, lymph glands, arteries, conjunctivae, and corneas. Hirsch (1982) reports the results of a “conventional” or non-stabilized vitamin D3 product being mixed into a trace mineral premix or into animal feed and stored at ambient room temperature (20°to 25°C) for up to 12 weeks. Thiamine is used for carbohydrate metabolism and energy production, and since it is not stored in the body, it needs to be constantly replenished. Vitamin D toxicity is enhanced by elevated supplies of dietary calcium and phosphorus and is reduced when the diet is low in calcium. Sommerfeldt et al. Endocr Connect. Vitamin D Deficiency. Turkey osteomyelitis, a disease that affects commercially produced turkeys and disease incidence in E. coli-challenged birds was also decreased with vitamin D metabolites (Huff et al., 2002). When standing, the elbows were slightly abducted and there was mild valgus deviation of the front paws. Excessive vitamin D concentrations may result in hypercalcemia, soft-tissue calcification and ultimately death (Nakamura et al., 2004). In the skin of the dog and cat the concentrations of the precursor 7-dehydrocholesterol are low and the precursor is inadequately converted to vitamin D. It is suggested that carnivores do not need to provide their own vitamin D, since fat, liver and blood of their prey will fulfill this need (How et al.,1995).Vitamin D requirements of cats and dogs are suggested to be sufficiently high to produce normal growth, calcification, production and reproduction, provided that diets contain recommended levels of calcium and available phosphorus. Once formed in the kidney, 1,25-(OH)2D is then transported to the intestine, bones or elsewhere in the body, where it is involved in the metabolism of calcium and phosphorus. The primary function of vitamin D is to elevate plasma calcium and phosphorus to a level that will support normal mineralization of bone as well as other body functions. Mushrooms provide variable amounts of vitamin D 2 [ 17 ]. 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