Disease relevance of Vitamin D Deficiency

• Megalin-/- mice are unable to retrieve the steroid from the glomerular filtrate and develop vitamin D deficiency and bone disease [1].
• Prolonged therapy with rifampicin or phenobarbital has been shown to cause vitamin D deficiency or osteomalacia, particularly in patients with marginal vitamin D stores [2].
• When maintained on vitamin D-deficient diets for a brief period, the DBP-/-, but not DBP+/+, mice developed secondary hyperparathyroidism and the accompanying bone changes associated with vitamin D deficiency [3].
• Hypocalcemia during sepsis occurred in previously normocalcemic patients and was multifactorial in origin, resulting from acquired parathyroid gland insufficiency, renal 1 alpha-hydroxylase insufficiency, vitamin D deficiency, and acquired calcitriol resistance [4].
• Although 1,25(OH)(2)D(3) up-regulates VDR expression, hypocalcemia and vitamin D deficiency result in drastically reduced expression of the receptor [5].

Psychiatry related information on Vitamin D Deficiency

• Thus, in Florida there is very little risk for vitamin D deficiency, and vitamin A and E status seems to be unaffected by differences in dietary habits [6].

High impact information on Vitamin D Deficiency

• Vitamin D deficiency and secondary hyperparathyroidism in the elderly: consequences for bone loss and fractures and therapeutic implications [7].
• The effects of a vitamin D deficiency on insulin and glucagon release was determined in the isolated perfused rat pancreas by radioimmunoassay of the secreted proteins [8].
• In this issue of the JCI, Pascussi et al. provide convincing evidence that PXR can also induce vitamin D deficiency and bone disease because of its ability to cross-talk with the vitamin D-responsive gene that catabolizes 25-hydroxy-vitamin D and 1,25-dihydroxyvitamin D [9].
• This cross-talk behavior has important health ramifications and can be mitigated through the identification and treatment of PXR-induced vitamin D deficiency [9].
• In vitamin D deficiency, there were no alterations in colonic PKC isoform expression but significant changes in the subcellular distribution of PKC-alpha, -delta, and -zeta [10].

Chemical compound and disease context of Vitamin D Deficiency

• Estrogen deficiency is known to play a critical role in the development of osteoporosis, while calcium and vitamin D deficiencies and secondary hyperparathyroidism also contribute [11].
• With the exception of a modest decrease in muscle creatine phosphate levels, muscle composition was unchanged by vitamin D deficiency [12].
• We conclude that oral 25-hydroxyvitamin D corrects vitamin D deficiency and reverses osteomalacia in primary biliary cirrhosis [13].
• It is suggested that the high frequency of vitamin-D deficiency in Asian adolescents would be much reduced if 1 mg of vitamin D3 was given orally each school term during adolescence [14].
• Furthermore, they demonstrate the effect of vitamin D deficiency and its reversal on plasma creatinine concentrations [15].

Biological context of Vitamin D Deficiency

• The aims of this study were to investigate the prevalence of vitamin D deficiency, as assessed by low serum concentrations of 25-hydroxyvitamin D (25(OH)D) in patients with small intestinal resection and to explore the relation of 25(OH)D to PTH, markers of bone turnover rate, and bone mineral density (BMD) in these patients [16].
• Recent studies suggest that secondary hyperparathyroidism and/or vitamin D deficiency are responsible for the insulin resistance in chronic renal failure [17].
• Sex differences during the development of vitamin D deficiency in the rat: serum parathyroid hormone, calcitonin, calcium, and phosphorus [18].
• In all groups Sm-C/IGF-I concentrations correlated well with food intake, indicating that calorie intake, and not vitamin D deficiency or hypocalcemia, was the primary factor in reducing Sm-C/IGF-I [19].
• It is, in part, due to increased endogenous glucocorticoids that contribute to the reduction in bone formation and osteoblast differentiation, hypercalciuria secondary to hypoparathyroidism, and vitamin D deficiency [20].

Anatomical context of Vitamin D Deficiency

• Vitamin D is a selective regulator of the immune system, and the outcome of 1,25(OH)2D3 treatment, vitamin D deficiency, or VDR deficiency depends on the nature of the immune response (eg, infectious disease, asthma, or autoimmune disease) [21].
• The adenosine triphosphate-dependent calcium pump in rat small intestine: effects of vitamin D deficiency and cell isolation methods [22].
• To examine its correlation with bone metabolism in a population of institutionalized elderly people known to be at high risk for vitamin D deficiency and secondary hyperparathyroidism, QUS of the calcaneus and biochemical parameters were measured in 264 women aged 85 +/- 7 (SD) years and in 103 men aged 81 +/- 8 years living in 19 nursing homes [23].
• Insulin secretion is impaired by vitamin D deficiency and is restored by 1,25-(OH)2D3 (concomitantly with an improved calcium handling within B cells) but the effect of 1,25-(OH)2D3 on the pancreatic B cell via calbindin-D is unclear [24].
• In conclusion, vitamin D-deficiency in vivo suppressed subsequent glucose-stimulated insulin release in vitro and this effect may be due to a direct effect of the sterol (or one of its metabolites) on calcium handling by the B cell [25].

Gene context of Vitamin D Deficiency

• These results suggest that chronic and profound hypocalcemia and/or vitamin D deficiency can stimulate endogenous PTHrP secretion via a negative feedback mechanism, although elevated iPTHrP does not normalize the decreased serum calcium levels [26].
• OBJECTIVE: To improve understanding of the biochemical events in vitamin D-deficiency rickets (VDR) [27].
• Aim: To examine the hypothesis that vitamin D status modulates the matrix metalloproteinase (MMP) system in a population with a high prevalence of vitamin D deficiency, a situation affecting susceptibility to CHD and diabetes [28].
• METHODS: Circulating MMP2,9, the inhibitor TIMP-1 and C-reactive protein (CRP) were measured during studies of vitamin-D deficiency as a risk factor for type 2 diabetes and CHD in 171 healthy British Bangladeshi adults, free of known diabetes or major illness [28].
• This favors the concept that vitamin D deficiency diminishes the activation of renal adenylate cyclase by PTH which is overcome by the highly increased PTH secretion in the advanced stages of rickets [29].

Analytical, diagnostic and therapeutic context of Vitamin D Deficiency

• This animal model was selected to mimic the situation observed in elderly women in whom estrogen deficiency and/or low-protein intake (but also calcium and vitamin D deficiency) are known to contribute to the pathogenesis of osteoporosis [30].
• In univariate analyses, risk factors for vitamin D deficiency included increasing age, black race, low educational level, high body mass index, high triceps skinfold thickness, increasing level of disability, winter season, and elevated creatinine concentration [31].
• Several clearance and micropuncture studies suggest that vitamin D deficiency decreases calcium (Ca2+) reabsorption by the nephron [32].
• Intravenous glucose tolerance tests were performed in Dutch rabbits (n = 12) before and after nutritional vitamin D deficiency, characterized by an absence of circulating 25-hydroxyvitamin D3, a 50% decrease in 1,25-dihydroxyvitamin D3, and a 16% decrease in serum calcium concentrations [33].
• An absence of skeletal complications, a survival beyond three months of age without parathyroidectomy and the masking of the hypercalcaemia by vitamin D deficiency represents a unique combination of metabolic abnormalities in a patient with neonatal primary hyperparathyroidism [34].

References