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Vitamin D in Canine Health
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Nobody ever said that vitamins are an easy subject to understand – and although they are essential for life, too much or too little of a vitamin can make a huge difference to an animal’s health. Valerie Parker makes it all clear in her excellent review of Vitamin D.
Valerie J. Parker
DVM, Dipl. ACVIM, Dipl. ACVN
Dr. Parker received her DVM from Tufts University and went on to complete a smallanimal internship at the Animal Medical Center in New York City. She then undertook asmall animal internal medicine residency at Iowa State University and a clinical nutritionresidency at Tufts University. She is currently associate professor at OSU, with researchinterests that include vitamin D status in chronic kidney disease and its relationship tonutrition management.
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Key Points
- Vitamin D metabolism is complex and is affected by numerous dietary and hormonal factors.
- Depending on the methodology used, vitamin D metabolite concentrations can vary dramatically, and interlaboratory results may not be comparable.
- Dietary vitamin D intake cannot predict a dog’s 25(OH)D status.
- Various forms of vitamin D supplementation exist, but it is not clear what the best form of supplementation is for most diseases.
Vitamin D synthesis and metabolism
In many species, the biosynthesis of vitamin D begins with exposure to UV light, whereby 7-dehydrocholesterol is transformed to previtamin D3 . Factors that affect synthesis of vitamin D3 include quantity and quality of the UV light, the animal’s coat type, and skin pigmentation. Dogs differ from humans (and many other species) in that they lack the ability to synthesize vitamin D3 in the skin, likely because of high activity of the enzyme 7-dehydrocholesterol-Δ7-reductase. For this reason, dogs require dietary supplementation with vitamin D to meet nutritional requirements. There are two dietary forms of vitamin D: cholecalciferol (vitamin D3 ), which typically comes from animal food sources, and ergocalciferol (vitamin D2), which typically comes from plant sources.
Vitamin D is supplied in commercial dog foods in the form of various ingredients (e.g., organ meat or oily fish products) and supplemental cholecalciferol. Current AAFCO1 recommendations for minimum and maximum amounts of dietary vitamin D intake are 125 IU and 750 IU per 1000 kilocalories, respectively. While the cholecalciferol concentration in most commercially available diets has minimal impact on a dog’s serum 25(OH)D concentration, it can, if given in high enough quantities (up to 2700 IU/kg body weight) impact serum 25(OH)D concentrations (1). Clinicians should be aware that this dose far exceeds the National Research Council (NRC) safe upper limit of 2.6 μg (i.e., 104 IU) per kg body weight (BW)0.75.
Once ingested, vitamin D is transported to the liver via the portal system and intestinal lymphatics (Figure 1). This process requires digestive enzymes, chylomicrons, bile acids, vitamin D-binding protein (VDBP), and transcalciferin. In the liver, cholecalciferol is hydroxylated by 25-hydroxylase to form 25(OH)D (also known as calcidiol or calcifediol), which binds to VDBP in the circulation. With a half-life of approximately 2 to 3 weeks, 25(OH)D is thought to be the most reliable indicator of systemic vitamin D status.
25(OH)D is then hydroxylated (by 1α-hydroxylase) to form 1,25(OH)2 D (also known as calcitriol), the most active naturally occurring vitamin D metabolite; this affects many target cells via a vitamin D receptor (VDR)–mediated mechanism (Figure 1). Calcitriol binds to the VDR much more readily (approximately 500 times) than vitamin D3 or 25(OH)D. This activation of 1,25(OH)2 D occurs predominantly in the kidneys but also in other tissues that express 1α-hydroxylase. In dogs, VDR expression has been identified in several tissues, especially the kidney, duodenum, skin, ileum, and spleen. Although the exact mechanism has not been completely elucidated, 1α-hydroxylase activity is tightly regulated by serum concentrations of calcium, parathormone (PTH), 1,25(OH)2 D, fibroblast growth factor 23 (FGF-23), and activity of the enzyme Klotho. Within cells, 1,25(OH)2 D can promote or suppress gene transcription and expression. Both 25(OH)D and 1,25(OH)2 D are inactivated via 24-hydroxylase to form 24,25(OH)2 D and 1,24,25-trihydroxyvitamin D respectively, and other metabolites (e.g., 25[OH]D-23,23 lactone) that are excreted in the urine and bile.
1 AAFCO – Association of American Feed Control Officials
Vitamin D roles
Classically, vitamin D is known for its influence on calcium-phosphorus homeostasis via the bone-parathyroid-kidney axis. However, vitamin D has multiple other effects throughout the body, as evidenced by the wide variety of cells that express the VDR. Actions induced by VDR activation in humans include differentiation of immune cells, reductions in inflammation and proteinuria, increased insulin secretion, and improvement of hematopoiesis. [...]
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