Vitamin D3 metabolism in a pig strain with pseudo vitamin D-deficiency rickets, type I

Kaune, R.; Harmeyer, J.

doi:10.1530/acta.0.1150345

Cited by 17 publications

(12 citation statements)

References 2 publications

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“…64,219 Concentrations of 1,25(OH) 2 D 3 in the blood were low but significantly above zero, whereas concentrations of 25(OH)D 3 and PTH were high. 64,104,219 Calcium-binding protein concentrations in the plasma and intestine were reduced, and no 25-hydroxyvitamin D 3 -1a-hydroxylase and 24-hydroxylase activity was found in renal homogenates. 64 At the molecular level, VDDR I in the Hannover pig is associated with one of two different deletions in the P450C1 coding region.…”

Section: Pigsmentioning

confidence: 99%

Vitamin D Metabolism and Rickets in Domestic Animals

2010

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Rickets and osteomalacia are increasing in prevalence in people because of cultural practices, breast-feeding, decreased sun exposure, and increased sunscreen usage. Several hereditary forms of rickets owing to either renal phosphate wasting or defects in vitamin D metabolism are also reported in people. Rickets is well recognized in domestic animals, but published reports are not always supported by microscopic findings, and diagnoses based on clinical signs and radiology are unreliable. Most cases in domestic animals are caused by dietary deficiency of either vitamin D or phosphorus, but occasional inherited forms are reported in pigs, sheep, cats, and dogs. There is variation between species in susceptibility to dietary vitamin D and phosphorus deficiency and in the ability to manufacture vitamin D in their skin. A number of mouse models have been discovered or created to study human skeletal diseases and skeletal homeostasis. With the discovery that vitamin D is involved in not only calcium and phosphorus homeostasis but also in the immune system and cancer, there is great potential for new and existing animal models to generate valuable information about vitamin D and its many functions. This review presents an overview of vitamin D metabolism and rickets in domestic and laboratory animals and makes comparisons where appropriate with the disease in humans. Keywords bone, rickets, vitamin D, phosphorus, genetic diseasesRickets is a classic metabolic bone disease of humans and animals, first described in the first and second centuries. 158,165 With the discovery that vitamin D could prevent rickets, the prevalence of this disease in developed countries plummeted; however, it still occurs. In fact, the prevalence of rickets and vitamin D insufficiency is increasing in people of all ages in the developed world, due in part to decreased sunlight exposure and widespread sunscreen usage. 88 The disease is well recognized in animals, but published reports are uncommon and sometimes confusing.The pathogenesis of rickets involves impaired mineralization of physeal and epiphyseal cartilage during endochondral ossification and of newly formed osteoid. Most cases in domestic animals are caused by dietary deficiency of either vitamin D or phosphorus, but occasional inherited forms are reported. 109,200 Osteomalacia is caused by a failure of newly formed osteoid to mineralize, but it occurs in adults after closure of growth plates. 109In this article, we review vitamin D metabolism and rickets, with reference to the disease in domestic animals but presenting comparison with the disease in humans where appropriate. Biology of Vitamin D Activation of Vitamin DVitamin D is available from two sources: isomerization of 7-dehydrocholesterol (7-DHC) in the skin to vitamin D 3 following exposure to ultraviolet light or from ingestion of vitamin D 2 or D 3 in the diet. Only a few foods, including cod liver oil and fatty fish such as salmon and sardines, naturally contain high concentrations of vitamin D 3 .49 Vitamin D 2 i...

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Section: Pigsmentioning

confidence: 99%

Vitamin D Metabolism and Rickets in Domestic Animals

2010

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“…The mutant animals suffer from an inherited autosomal recessive defect of renal calcitriol synthesis (Winkler, Schreiner & Harmeyer, 1986) which leads to significantly lower calcitriol concentrations in plasma (Kaune & Harmeyer, 1987) and of calbindin concentrations in intestinal mucosa (Fox,452 Maunder, Randall & Care, 1985 The piglets were killed by stunning and bleeding. Three to five minutes after exsanguination jejunal segments of 1-5 m length were removed from the abdominal cavity beginning 1-0 m distal from the entry of the pancreatic duct.…”

Section: Introductionmentioning

confidence: 99%

Effects of calcitriol on stimulation of ion transport in pig jejunal mucosa.

Schröder

Kaune

Harmeyer

1991

The Journal of Physiology

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SUMMARY1. Active sodium (Na+) and chloride (Cl-) 5. Blocking Ca2+ entry into the cytosol by adding either 0-1 mM-TMB-8 or 0-5 mMd,l-verapamil to the serosal bathing solution abolished the difference in ISC response to theophylline between indomethacin-treated LC and NC mucosa due to greater depression of I., in LC than in NC mucosa.6. The combined effects of theophylline and A23187 on ISC stimulation were calcitriol dependent. In the presence of indomethacin this dependence was only significant when A23187 was given prior to theophylline. In the absence of indomethacin the combined effects of A23187 and theophylline on ISC were always significantly greater in LC than in NC mucosa, irrespective of the order of adding the two agents.7. Addition of theophylline stimulated net Na+ and Cl-secretion in indomethacintreated LC and NC mucosa. The increases of net Na+ and Cl-fluxes fully accounted for the rise of ISC with NC mucosa but accounted only partly for the increase in I., with LC mucosa. This resulted in significant increase in theophylline-stimulated MS 8176 15-2 B. SCHRODER, R. KA UNE AND J. HARMEYER residual ion flux (JR) in LC mucosa which probably resulted from enhanced secretion of bicarbonate.8. The experiments showed that in pig jejunal mucosa stimulation of ISC and ion transport by theophylline requires Ca2 . Greater stimulation of ISC in LC mucosa than in NC mucosa is explained by assuming a lower cytosolic Ca2+-buffering capacity. This probably resulted from the lower calbindin concentration in LC mucosa.9. The study shows that calcitriol alters responsiveness of the jejunal mucosa to Ca2+-dependent secretory stimuli.

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“…These piglets spontaneously develop severe hypocalcemia and hypophosphatemia [16]. The clinical symptoms are similar to those seen in humans with pseudo Vitamin D deficiency rickets, type I (PDDR-I).…”

Section: Animals and Dietsmentioning

confidence: 52%

“…Pigs are regarded a suitable model for the study of problems related to human nutrition. In a porcine animal model with inherited calcitriol deficiency [16] we have investigated whether high calcium and phosphate diets with casein as a protein source and a high lactose content, similar to those used in rats [11] can normalize calcium metabolism in calcitriol deficient pigs.…”

Section: Introductionmentioning

confidence: 99%