Vitamin D metabolism in canine and feline medicine
In many species, the biosynthesis of vitamin D begins with exposure to UV light, wherein 7-dehydrocholesterol is transformed to previtamin D3. Factors that affect synthesis of vitamin D3 include quantity and quality of the UV light, coat, and skin pigmentation. Dogs and cats are unique 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 7-dehydrocholesterol-Δ7-reductase.1,2 For this reason, dogs and cats require dietary supplementation with vitamin D to meet nutritional requirements. There are 2 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. Cats may not utilize ergocalciferol as efficiently as cholecalciferol3; however, dogs have the ability to utilize both dietary forms equally.4,a
Dietary vitamin D is supplied in commercially available dog and cat foods in the form of various ingredients (eg, organ meat or oily fish products) and supplemental cholecalciferol. Once ingested, it is transported to the liver via the portal system and intestinal lymphatics (Figure 1). This process requires digestive enzymes, chylomicrons, bile acids, and VDBP or transcalciferon.5,6 After cholecalciferol is transported to the liver, it 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 in humans.7
Then, 25(OH)D is hydroxylated via 1α-hydroxylase to form 1,25(OH)2D (the most active naturally occurring vitamin D metabolite; also known as calcitriol), which affects many target cells via a vitamin D receptor–mediated mechanism. Calcitriol binds to the vitamin D receptor much more readily (approx 500 times as readily) than does vitamin D3 or 25(OH)D.8 This activation of 1,25(OH)2D occurs predominately in the kidneys; however, it also occurs in other tissues that express 1α-hydroxylase. Although the exact mechanism has not been completely elucidated, 1α-hydroxylase activity is tightly regulated by serum concentrations of calcium, PTH, 1,25(OH)2D, FGF-23, and the Klotho gene.9–12 Within cells, 1,25(OH)2D can promote or suppress gene transcription and expression.13 Both 25(OH)D and 1,25(OH)2D are inactivated via 24-hydroxylase to form 24,25(OH)2D and 1,24,25-trihydroxyvitamin D, respectively, and other metabolites (eg, 25[OH]D-23,23 lactone) that are excreted in the urine and bile.14
A novel vitamin D epimer, which was identified as a C-3 epimer of 25(OH)D, has recently been discovered in cats by use of high-performance liquid chromatography.b Serum concentrations ranged from 18 to 30 ng/mL, which represented 29% to 75% of native 25(OH)D. This epimer has not been identified in dogs.
Authors: Valerie J. Parker, Adam J. Rudinsky, Dennis J. Chew
Source: https://avmajournals.avma.org/
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