Vitamin D deficiency influences fatty acid metabolism

Nandi, Anindita; Wadhwani, Nisha; Joshi, Sadhana

doi:10.1016/j.plefa.2018.11.014

Cited by 25 publications

(27 citation statements)

References 39 publications

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“…The body weight of the dams at the beginning of pregnancy (control: 198.50 ± 6.40 g; VDD: 198.13 ± 5.60 g) and at day 20 (control: 327.63 ± 26.44 g; VDD: 314.88 ± 12.30 g) were similar in both VDD and control groups. The litter weight and litter size were similar in both the groups . The fetal weight at day 20 was also similar (control: 3.05 ± 0.6 g; VDD: 3.00 ± 0.30 g) and has been reported by us earlier .…”

Section: Resultssupporting

confidence: 88%

“…The litter weight and litter size were similar in both the groups . The fetal weight at day 20 was also similar (control: 3.05 ± 0.6 g; VDD: 3.00 ± 0.30 g) and has been reported by us earlier .…”

Section: Resultssupporting

confidence: 88%

“…The serum levels of 25-hydroxyvitamin D3 at the end of pregnancy in the VDD group were lower as compared to the control group (P < 0.001; control: 44.70 AE 5.16 ng/mL; VDD: 9.22 AE 3.0 ng/mL) and have been reported by us earlier [30]. In the present study, vitamin D deficiency resulted in high PTH and low phosphate levels in dam serum as compared to the control group.…”

Section: Discussionsupporting

confidence: 74%

“…In our recent animal study, we observed an increase in the dam plasma and liver AA levels; although there was no change in the levels of placental AA in the VDD group as compared to control . Earlier reports in humans indicate that increase in the plasma AA levels is associated with an increase in the activity of COX and increase in the synthesis of TXB 2 .…”

Section: Discussionsupporting

confidence: 39%

“…In our recent animal study, we observed an increase in the dam plasma and liver AA levels; although there was no change in the levels of placental AA in the VDD group as compared to control [30]. Earlier reports in humans indicate that increase in the plasma FIG 4 Effect of vitamin D deficiency on fatty acid metabolism through one-carbon cycle; AA: arachidonic acid; sPLA 2 : secreted phospholipase A 2 ; PG: prostaglandin; TX: thromboxane; COX: cyclooxygenase; CBS: cystathionine-β-synthase; THF: tetrahydrofolate; 5-MTHF: 5-methyltetrahydrofolate; ROS: reactive oxygen species AA levels is associated with an increase in the activity of COX and increase in the synthesis of TXB 2 [61].…”

Section: Discussionmentioning

confidence: 57%

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Maternal vitamin D deficiency increases the thromboxane/prostacyclin ratio through alterations in the one‐carbon cycle in Wistar rats

2019

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This study aims to test the hypothesis that vitamin D deficiency can influence long‐chain polyunsaturated fatty acid metabolism through alterations in the one‐carbon cycle. Wistar rats (n = 8 per group) were given either a control (1,000 IU D3/kg diet) or a vitamin D deficient (VDD) (0 IU D3/kg diet) diet from pre‐pregnancy to delivery. On day 20 of gestation, pregnant female rats were delivered by C‐section to collect placenta and blood. VDD group demonstrated high serum parathyroid hormone, low serum phosphate, low plasma folate, higher plasma homocysteine, and higher plasma malondialdehyde levels (P < 0.05 for all) as compared to control. Lower protein levels of placental cystathionine‐β‐synthase enzyme (P < 0.05) were observed in the VDD group as compared to control. VDD group demonstrated higher placental mRNA levels of the enzymes phospholipase A2 and cyclooxygenase‐2 (P < 0.05 for both) as compared to control. Protein levels of the enzymes phospholipase A2 and cyclooxygenase‐2 were lower (P < 0.05 for both) in the VDD group as compared to the control group. The ratio of thromboxane B2 and 6‐keto prostaglandin F1α in serum was higher (P < 0.05) in the VDD group as compared to control; although the serum levels of 6‐keto prostaglandin F1α and thromboxane B2 were similar in both the groups. Our findings suggest that increased oxidative stress due to maternal vitamin D deficiency results in the imbalance between the vasoconstrictor (thromboxane B2) and vasodilator (6‐keto prostaglandin F1α) eicosanoids, which may lead to endothelial dysfunction and poor pregnancy outcome. © 2019 BioFactors, 45 (4):548–555, 2019

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Section: Resultssupporting

confidence: 88%

Section: Resultssupporting

confidence: 88%

Section: Discussionsupporting

confidence: 74%

“…In our recent animal study, we observed an increase in the dam plasma and liver AA levels; although there was no change in the levels of placental AA in the VDD group as compared to control . Earlier reports in humans indicate that increase in the plasma AA levels is associated with an increase in the activity of COX and increase in the synthesis of TXB 2 .…”

Section: Discussionsupporting

confidence: 39%

“…In our recent animal study, we observed an increase in the dam plasma and liver AA levels; although there was no change in the levels of placental AA in the VDD group as compared to control [30]. Earlier reports in humans indicate that increase in the plasma FIG 4 Effect of vitamin D deficiency on fatty acid metabolism through one-carbon cycle; AA: arachidonic acid; sPLA 2 : secreted phospholipase A 2 ; PG: prostaglandin; TX: thromboxane; COX: cyclooxygenase; CBS: cystathionine-β-synthase; THF: tetrahydrofolate; 5-MTHF: 5-methyltetrahydrofolate; ROS: reactive oxygen species AA levels is associated with an increase in the activity of COX and increase in the synthesis of TXB 2 [61].…”

Section: Discussionmentioning

confidence: 57%

See 3 more Smart Citations

Maternal vitamin D deficiency increases the thromboxane/prostacyclin ratio through alterations in the one‐carbon cycle in Wistar rats

2019

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Vitamin D status and latitude predict brain lesions in adrenoleukodystrophy

Haren

Wilkes

Moser

et al. 2023

Annals of the Child Neurology Society

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Objectives: Approximately 40% of boys with X-linked adrenoleukodystrophy (ALD) develop inflammatory demyelinating brain lesions (cerebral ALD, cALD) and are at risk for death or severe disability. Risk factors for cALD are poorly understood. Our objective was to evaluate whether vitamin D status, which influences immune function, is associated with risk for cALD. Methods: We used two independent cohorts to assess whether low vitamin D status is correlated with cALD. We used complementary proxies for vitamin D status: plasma 25-hydroxyvitamin D levels and latitude. In our first cohort, we measured 25-hydroxyvitamin D in biobanked plasma samples from ALD boys with initially normal brain MRIs followed at two expert centers. In a second cohort, we measured latitude (using home ZIP code) among ALD boys identified in a national administrative database (PHIS) covering 51 US pediatric hospitals. We used logistic regression models to estimate the odds of developing cALD in each cohort. Results: In the first cohort, we identified 20 ALD boys with a total of plasma sample timepoints who met inclusion criteria; 50% (n = 10) subsequently developed cALD. Average 25-hydroxyvitamin D levels were lower among boys who developed cALD than those who did not (median 28.9 vs 36.6 ng/ml); p = 0.019. For each 10 ng/mL decrease in 25-hydroxyvitamin D, the odds ratio for developing cALD was 6.94; p = 0.044. In the second cohort, we identified ALD boys across 28 states; 57% of boys (n = 132) developed cALD. Each 2°i ncrease in latitude conferred an odds ratio of 1.17 (95% confidence interval, 1.01, 1.35); p = 0.036 for developing cALD. Conclusions: Using independent cohorts, we found that ALD boys with lower pre-morbid plasma levels of 25-hydroxyvitamin D, or more northerly latitude of residence, were more likely to develop cALD. These findings offer complementary lines of evidence that vitamin D and/or ultraviolet light exposure influence cALD risk.

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