Browsing by Subject "vitamin D deficiency"

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  • Mäkitaipale, Johanna; Sievänen, Harri; Sankari, Satu; Vapaavuori, Outi (2019)
    During the winter time in Finland, sunlight is inadequate for vitamin D synthesis. Many pet rabbits live as house rabbits with limited outdoor access even during summer and may therefore be dependent on dietary sources of vitamin D. The aims of this study were to report the serum 25-hydroxyvitamin D concentrations in Finnish pet rabbits and to identify factors that influence vitamin D status. Serum 25-hydroxyvitamin D concentrations from 140 pet rabbits were determined using a vitamin D enzyme immunoassay (EIA) kit. Eleven rabbits were excluded from the statistical analysis because of unclear dietary data. The remaining 129 rabbits were divided into groups depending on outdoor access during summer (no access n = 26, periodic n = 57, regular n = 46) as well as daily diet: little or no hay and commercial rabbit food = 1 dl (n = 35). The range of serum 25-hydroxyvitamin D concentration was from 4.5 to 67.5 ng/ml with a mean of 26.1 ng/ml. Statistical general linear model adjusted for weight, age and season indicated that diet was associated with vitamin D concentrations (p = 0.001), but outdoor access during summer was not (p = 0.41). Mean 25-hydroxyvitamin D concentration was significantly higher in the rabbits receiving a lot of hay and commercial food >= 1 dl (33.9 +/- 13.2 ng/ml) than in rabbits in other diet groups (24.0 +/- 8.5 ng/ml, 21.7 +/- 8.1 ng/ml, and 22.2 +/- 18.0 ng/ml, respectively). This investigation showed wide variation in 25-hydroxyvitamin D concentrations among Finnish pet rabbits. Diet remains a main source since outdoor access seems to be too limited to provide adequate vitamin D synthesis for most of them, and the use of vitamin D supplements is rare.
  • Beck-Nielsen, Signe Sparre; Mughal, Zulf; Haffner, Dieter; Nilsson, Ola; Levtchenko, Elena; Ariceta, Gema; Collantes, Carmen de Lucas; Schnabel, Dirk; Jandhyala, Ravi; Mäkitie, Outi (2019)
    Background: X-linked hypophosphatemia (XLH) is an inherited disease of phosphate metabolism in which inactivating mutations of the Phosphate Regulating Endopeptidase Homolog, X-Linked (PHEX) gene lead to local and systemic effects including impaired growth, rickets, osteomalacia, bone abnormalities, bone pain, spontaneous dental abscesses, hearing difficulties, enthesopathy, osteoarthritis, and muscular dysfunction. Patients with XLH present with elevated levels of fibroblast growth factor 23 (FGF23), which is thought to mediate many of the aforementioned manifestations of the disease. Elevated FGF23 has also been observed in many other diseases of hypophosphatemia, and a range of animal models have been developed to study these diseases, yet the role of FGF23 in the pathophysiology of XLH is incompletely understood. Methods: The role of FGF23 in the pathophysiology of XLH is here reviewed by describing what is known about phenotypes associated with various PHEX mutations, animal models of XLH, and non-nutritional diseases of hypophosphatemia, and by presenting molecular pathways that have been proposed to contribute to manifestations of XLH. Results: The pathophysiology of XLH is complex, involving a range of molecular pathways that variously contribute to different manifestations of the disease. Hypophosphatemia due to elevated FGF23 is the most obvious contributor, however localised fluctuations in tissue non-specific alkaline phosphatase (TNAP), pyrophosphate, calcitriol and direct effects of FGF23 have been observed to be associated with certain manifestations. Conclusions: By describing what is known about these pathways, this review highlights key areas for future research that would contribute to the understanding and clinical treatment of non-nutritional diseases of hypophosphatemia, particularly XLH.
  • Beck-Nielsen, Signe S; Mughal, Zulf; Haffner, Dieter; Nilsson, Ola; Levtchenko, Elena; Ariceta, Gema; de Lucas Collantes, Carmen; Schnabel, Dirk; Jandhyala, Ravi; Mäkitie, Outi (BioMed Central, 2019)
    Abstract Background X-linked hypophosphatemia (XLH) is an inherited disease of phosphate metabolism in which inactivating mutations of the Phosphate Regulating Endopeptidase Homolog, X-Linked (PHEX) gene lead to local and systemic effects including impaired growth, rickets, osteomalacia, bone abnormalities, bone pain, spontaneous dental abscesses, hearing difficulties, enthesopathy, osteoarthritis, and muscular dysfunction. Patients with XLH present with elevated levels of fibroblast growth factor 23 (FGF23), which is thought to mediate many of the aforementioned manifestations of the disease. Elevated FGF23 has also been observed in many other diseases of hypophosphatemia, and a range of animal models have been developed to study these diseases, yet the role of FGF23 in the pathophysiology of XLH is incompletely understood. Methods The role of FGF23 in the pathophysiology of XLH is here reviewed by describing what is known about phenotypes associated with various PHEX mutations, animal models of XLH, and non-nutritional diseases of hypophosphatemia, and by presenting molecular pathways that have been proposed to contribute to manifestations of XLH. Results The pathophysiology of XLH is complex, involving a range of molecular pathways that variously contribute to different manifestations of the disease. Hypophosphatemia due to elevated FGF23 is the most obvious contributor, however localised fluctuations in tissue non-specific alkaline phosphatase (TNAP), pyrophosphate, calcitriol and direct effects of FGF23 have been observed to be associated with certain manifestations. Conclusions By describing what is known about these pathways, this review highlights key areas for future research that would contribute to the understanding and clinical treatment of non-nutritional diseases of hypophosphatemia, particularly XLH.
  • Reinert, Linnea (Helsingfors universitet, 2010)
    Vitamin D is either obtained through synthesis in the skin due to UVB-light (290-315 nm) or from the diet. The hydroxylased metabolite 25-hydroxyvitamin D (25(OH)D) is the metabolite to measure when vitamin D status wants to be determined. The active form of vitamin D is 1,25- dihydroxyvitamin D (1,25(OH)?D) which interacts with a large set of tissue cells (especially bone) through its nuclear receptor the vitamin D receptor (VDR). Vitamin D deficiency can lead to rickets in children and osteoporosis or osteomalacia in adults. Type 1 Diabetes (T1D) is an autoimmune disease which is caused by the destruction of the pancreatic ?-cells. The disease has genetic and environmental features but the whole mechanism of disease development is still unknown. The prevalence of T1D is constantly growing in the whole world. Therefore it is important to study possible environmental factors that can eventually serve as pathogenesis modifiers. Vitamin D and T1D have been associated among others because there is a seasonal and geographical variation in T1D incidence, more cases have been identified in the North and during winter. The aim of this study was to investigate if the serum 25(OH)D status during first trimester of pregnancy is associated with T1D development in the offspring. The subjects where mothers of T1D children (N=310) and the controls were mothers of healthy children (N=310). Serum samples were obtained from the Finnish Maternity Cohort (FMC) and analyzed for S-25(OH)D. S- 25(OH)D measurement was performed with an indirect enzyme immunoassay (EIA). No significant (p>0.05) difference was seen between S-25(OH)D mean concentrations in cases and controls. The mean concentration of cases was 43.3 ± 15.9 nmol/l and 43.0 ± 15.5 nmol/l (mean ± standard deviation (SD)) of controls. Insufficient and deficient S- 25(OH)D status was seen in 72% of the whole study population. As a result of this study it has been shown that the S-25(OH)D status during first trimester of pregnancy is not associated with T1D development in the offspring. Samples from later stages of pregnancy could be analyzed to determine if the overall status during pregnancy has an effect on T1D development in the offspring. Considering the possible health outcomes of vitamin D insufficiency, recommended vitamin D supplementation should be raised to improve maternal and fetal health.