scholarly journals Combined Treatment with Omega-3 Fatty Acid and Cholecalciferol Increases 1,25-Dihydroxyvitamin D Levels by Modulating Dysregulation of Vitamin D Metabolism in 5/6 Nephrectomy Rats

Nutrients ◽  
2019 ◽  
Vol 11 (12) ◽  
pp. 2903
Author(s):  
Su Mi Lee ◽  
Mi Hwa Lee ◽  
Young Ki Son ◽  
Seong Eun Kim ◽  
Won Suk An
Keyword(s):  
Vitamin D ◽  
Fatty Acid ◽  
Combined Treatment ◽  
Omega 3 ◽  
Sprague Dawley ◽  
Vitamin D Metabolism ◽  
Omega 3 Fatty Acid ◽  
Hydroxyvitamin D ◽  
Dihydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D

The protein 1α-hydroxylase (CYP27B1) was expressed in liver and omega-3 fatty acid (FA) elevated 1,25-dihydroxyvitamin D [1,25(OH)2D] levels in dialysis patients. The aim of this study was to determine whether omega-3 FA and cholecalciferol have effects on vitamin D metabolism related to CYP27B1 and 24-hydroxylase (CYP24) activities in the kidney and liver of 5/6 nephrectomy (Nx) rats. Male Sprague–Dawley rats were divided into the following groups: sham control, 5/6 Nx, 5/6 Nx treated with cholecalciferol, 5/6 Nx treated with omega-3 FA, and 5/6 Nx treated with cholecalciferol/omega-3 FA. CYP27B1 and CYP24 expression were measured in the liver and kidney. Further, 1,25(OH)2D and 25-hydroxyvitamin D [25(OH)D] levels were measured in serum. Among Nx groups, 1,25(OH)2D and 25(OH)D levels were lowest in the 5/6 Nx group. CYP24 expression was increased in the kidney of the 5/6 Nx rat model, which was found to be reversed by omega-3 FA or cholecalciferol/omega-3 FA supplementation. Decreased CYP27B1 expression was observed in the liver of the 5/6 Nx rats and its expression was recovered by supplementation with cholecalciferol/omega-3 FA. In conclusion, omega-3 FA and cholecalciferol may synergistically increase 1,25(OH)2D levels by inhibiting CYP24 expression in the kidney and liver and activating CYP27B1 expression in the liver of 5/6 Nx rats.

Omega-3 fatty acid supplementation increases 1,25-dihydroxyvitamin D and fetuin-A levels in dialysis patients

2012 ◽  
Vol 32 (7) ◽  
pp. 495-502 ◽  
Author(s):  
Won Suk An ◽  
Su Mi Lee ◽  
Young Ki Son ◽  
Seong Eun Kim ◽  
Ki Hyun Kim ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Omega 3 ◽  
Dialysis Patients ◽  
Fatty Acid Supplementation ◽  
Fetuin A ◽  
Acid Supplementation ◽  
Omega 3 Fatty Acid ◽  
Dihydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D

scholarly journals Plasma 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D, and parathyroid hormone in familial hypocalciuric hypercalcemia and primary hyperparathyroidism

2008 ◽  
Vol 159 (6) ◽  
pp. 719-727 ◽  
Author(s):  
Signe Engkjær Christensen ◽  
Peter H Nissen ◽  
Peter Vestergaard ◽  
Lene Heickendorff ◽  
Lars Rejnmark ◽  
...  
Keyword(s):  
Vitamin D ◽  
Parathyroid Hormone ◽  
Primary Hyperparathyroidism ◽  
Plasma Levels ◽  
Familial Hypocalciuric Hypercalcemia ◽  
Vitamin D Metabolism ◽  
Hydroxyvitamin D ◽  
Dihydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D ◽  
25 Hydroxyvitamin D

IntroductionFamilial hypocalciuric hypercalcemia (FHH) is a lifelong, benign, inherited condition caused by inactivating mutations in the calcium-sensing receptor (CASR) gene. Both FHH and primary hyperparathyroidism (PHPT) are characterized by elevated P-calcium, normal or elevated plasma-parathyroid hormone (P-PTH), and typically normal renal function. In PHPT, vitamin D metabolism is typically characterized by low plasma levels of 25-hydroxyvitamin D (25OHD), and high plasma levels of 1,25-dihydroxyvitamin D (1,25(OH)2D). In FHH, the vitamin D metabolism is not very well known.ObjectiveTo compare and evaluate plasma 25OHD, 1,25(OH)2D, and PTH in FHH and PHPT.DesignCross-sectional study.MaterialsAbout 66 FHH patients with mutations in the CASR gene, 147 patients with surgically verified PHPT, and 46 controls matched to FHH patients according to age (±5 years), sex, and season. All patients had a P-creatinine <140 μmol/l.MethodsWe measured P-calcium, P-Ca2+, P-albumin, P-creatinine, P-phosphate, P-magnesium, and P-PTH by standard laboratory methods. P-25OHD and P-1,25(OH)2D were measured by RIA or enzyme immunoassay. In FHH, all protein-coding exons in the CASR gene were sequenced and aligned to GenBank reference sequence .ResultsPHPT patients had higher body mass index (2p<0.01), together with higher P-PTH (2p<0.01) and P-1,25(OH)2D (2p<0.01) compared with FHH patients. The groups had similar levels of P-Ca2+ and of P-25OHD. The phenotypic expression of the CASR mutations (as determined by the degree of hypercalcemia) did not influence the levels of P-1,25(OH)2D.ConclusionEven though P-calcium and P-25OHD were comparable, P-1,25(OH)2D and P-PTH differed between FHH and PHPT.

Vitamin D

2005 ◽  
Vol 289 (1) ◽  
pp. F8-F28 ◽  
Author(s):  
Adriana S. Dusso ◽  
Alex J. Brown ◽  
Eduardo Slatopolsky
Keyword(s):  
Vitamin D ◽  
Target Genes ◽  
Endocrine System ◽  
Target Cells ◽  
Vitamin D Metabolism ◽  
Diverse Range ◽  
Hydroxyvitamin D ◽  
Dihydroxyvitamin D ◽  
Single Receptor ◽  
Recent Developments

The vitamin D endocrine system plays an essential role in calcium homeostasis and bone metabolism, but research during the past two decades has revealed a diverse range of biological actions that include induction of cell differentiation, inhibition of cell growth, immunomodulation, and control of other hormonal systems. Vitamin D itself is a prohormone that is metabolically converted to the active metabolite, 1,25-dihydroxyvitamin D [1,25(OH)2D]. This vitamin D hormone activates its cellular receptor (vitamin D receptor or VDR), which alters the transcription rates of target genes responsible for the biological responses. This review focuses on several recent developments that extend our understanding of the complexities of vitamin D metabolism and actions: the final step in the activation of vitamin D, conversion of 25-hydroxyvitamin D to 1,25(OH)2D in renal proximal tubules, is now known to involve facilitated uptake and intracellular delivery of the precursor to 1α-hydroxylase. Emerging evidence using mice lacking the VDR and/or 1α-hydroxylase indicates both 1,25(OH)2D3-dependent and -independent actions of the VDR as well as VDR-dependent and -independent actions of 1,25(OH)2D3. Thus the vitamin D system may involve more than a single receptor and ligand. The presence of 1α-hydroxylase in many target cells indicates autocrine/paracrine functions for 1,25(OH)2D3in the control of cell proliferation and differentiation. This local production of 1,25(OH)2D3is dependent on circulating precursor levels, providing a potential explanation for the association of vitamin D deficiency with various cancers and autoimmune diseases.

Protective effects of dietary omega-3 fatty acid supplementation on organophosphate poisoning

2017 ◽  
Vol 34 (2) ◽  
pp. 69-82 ◽  
Author(s):  
Bahattin Avci ◽  
S. Sirri Bilge ◽  
Gokhan Arslan ◽  
Omer Alici ◽  
Ozge Darakci ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Olive Oil ◽  
The Body ◽  
Control Group ◽  
Organophosphate Poisoning ◽  
Protective Effects ◽  
Omega 3 ◽  
Sprague Dawley ◽  
Omega 3 Fatty Acid ◽  
Locomotor Activities

In this study, we aimed to study the possible preventive effect of docosahexaenoic acid (DHA), a dietary omega-3 fatty acid, on toxicity caused by chlorpyrifos (CPF). Six groups of Sprague Dawley rats (200–250 g) consisting of equal numbers of males and females (n = 8) were assigned to study. The rats were orally given for 5 days. The control group was administered pure olive oil, which was the vehicle for CPF. The CPF challenge groups were administered oral physiological saline, pure olive oil, or DHA (50, 100 and 400 mg/kg dosages) for 5 days. The animals were weighed on the sixth day and then administered CPF (279 mg/kg, subcutaneously). The rats were weighed again 24 h following CPF administration. The body temperatures and locomotor activities of the rats were also measured. Blood samples, brain and liver tissues were collected for biochemical, histopathological and immunohistochemical examinations. A comparison with the control group demonstrated that CPF administration increased malondialdehyde (MDA) levels in blood, brain and liver, while it reduced catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPx) concentrations ( p < 0.05–0.001). Advanced oxidation protein products (AOPPs) increased only in the brain ( p < 0.001). DHA reduced these changes in MDA and AOPP values ( p < 0.05–0.001), while it increased CAT, SOD and GPx concentrations ( p < 0.05–0.001). Similarly, DHA prevented the decreases in body weight, body temperature and locomotor activities caused by CPF at 100 mg/kg and 400 mg/kg dosages ( p < 0.05–0.001). Similar to the physiological and biochemical changes, the histopathological damage scores, which increased with CPF ( p < 0.05–0.01), decreased at all three dosages of DHA ( p < 0.05–0.01). Our findings suggest that DHA, by supporting the antioxidant mechanism, reduces toxicity caused by CPF.

Extrarenal synthesis of 1,25-dihydroxyvitamin D: Sensitivity to glucocorticoid treatment

1987 ◽  
Vol 72 (3) ◽  
pp. 329-334 ◽  
Author(s):  
Silvano Adami ◽  
G. Graziani ◽  
D. Tartarotti ◽  
R. Cappelli ◽  
S. Casati ◽  
...  
Keyword(s):  
Vitamin D ◽  
Serum Calcium ◽  
Glucocorticoid Treatment ◽  
Prednisone Therapy ◽  
Hydroxyvitamin D ◽  
Dihydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D ◽  
Prednisone Treatment ◽  
Vitamin D Intoxication ◽  
Before And After

1. The response of circulating 1,25-dihydroxyvitamin D [l,25-(OH)2D] to challenge with vitamin D treatment both before and after 7–10 days of prednisone therapy (25 mg/day) was investigated in five anephric subjects, six patients with chronic renal failure (CRF), two patients with vitamin D intoxication and four patients with hypoparathyroidism. 2. In anephric subjects serum 25-hydroxyvitamin D [25-(OH)D] rose from 58 ± 48 (sd) to 377±221 (sd) nmol/l after administration of 150 μg of 25-(OH)D3 for 1 month. Serum l,25-(OH)2D, which was barely detectable in only two out of five patients under basal conditions, rose to 30 ± 21 pmol/l after 2 weeks of therapy with 25-(OH)D3, but fell to 10 ± 5 pmol/l during prednisone treatment. 3. In CRF patients circulating l,25-(OH)2D rose from 37 ± 24 to 58 ± 24 pmol/l during 25-(OH)D3 therapy, but fell to 41 ± 31 pmol/l during prednisone treatment. In two patients with rheumatoid arthritis, hypercalcaemia due to vitamin D intoxication was associated with raised levels of 1,25-(OH)2D (288 and 317 pmol/l). Administration of prednisore resulted in suppression of l,25-(OH)2D levels (132 and 96 pmol/l respectively) and reduction of serum calcium to within the normal range. 4. In the hypoparathyroid patients prednisone therapy did not affect circulating 25-(OH)D levels but serum l,25-(OH)2D fell from 192 ± 42 to 117 ± 23 pmol/l and serum calcium from 2.41 ± 0.21 to 2.20 ± 0.05 mmol/l. 5. These findings indicate that a steroid sensitive extrarenal production of l,25-(OH)2D may occur in all subjects with a threshold serum concentration of the precursor 25-(OH)D.

scholarly journals The Effects of Omega-3 Fatty Acid on Vitamin D Activation in Hemodialysis Patients: A Pilot Study

Marine Drugs ◽  
2015 ◽  
Vol 13 (2) ◽  
pp. 741-755 ◽  
Author(s):  
Su Lee ◽  
Young Son ◽  
Seong Kim ◽  
Won An
Keyword(s):  
Vitamin D ◽  
Fatty Acid ◽  
Pilot Study ◽  
Hemodialysis Patients ◽  
Omega 3 ◽  
Omega 3 Fatty Acid
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