Effect of nutritional vitamin A deficiency on lipid metabolism in the rat heart: Its relation to PPAR gene expression

Nutrition ◽  
2009 ◽  
Vol 25 (7-8) ◽  
pp. 828-838 ◽  
Author(s):  
Verónica Analía Vega ◽  
Ana Cecilia Anzulovich ◽  
Silvia Mabel Varas ◽  
Mirtha Ruth Bonomi ◽  
María Sofía Giménez ◽  
...  
Keyword(s):  
Gene Expression ◽  
Lipid Metabolism ◽  
Vitamin A ◽  
Rat Heart ◽  
Vitamin A Deficiency ◽  
Nutritional Vitamin

scholarly journals CMO1 Deficiency Abolishes Vitamin A Production from β-Carotene and Alters Lipid Metabolism in Mice

2007 ◽  
Vol 282 (46) ◽  
pp. 33553-33561 ◽  
Author(s):  
Susanne Hessel ◽  
Anne Eichinger ◽  
Andrea Isken ◽  
Jaume Amengual ◽  
Silke Hunzelmann ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Vitamin A ◽  
Vitamin A Deficiency ◽  
Elevated Serum ◽  
Pcr Analysis ◽  
Marker Genes ◽  
Mouse Mutant ◽  
Adipose Tissues ◽  
Β Carotene

Carotenoids are currently investigated regarding their potential to lower the risk of chronic disease and to combat vitamin A deficiency in humans. These plant-derived compounds must be cleaved and metabolically converted by intrinsic carotenoid oxygenases to support the panoply of vitamin A-dependent physiological processes. Two different carotenoid-cleaving enzymes were identified in mammals, the classical carotenoid-15,15′-oxygenase (CMO1) and a putative carotenoid-9′,10′-oxygenase (CMO2). To analyze the role of CMO1 in mammalian physiology, here we disrupted the corresponding gene by targeted homologous recombination in mice. On a diet providing β-carotene as major vitamin A precursor, vitamin A levels fell dramatically in several tissues examined. Instead, this mouse mutant accumulated the provitamin in large quantities (e.g. as seen by an orange coloring of adipose tissues). Besides impairments in β-carotene metabolism, CMO1 deficiency more generally interfered with lipid homeostasis. Even on a vitamin A-sufficient chow, CMO1-/- mice developed a fatty liver and displayed altered serum lipid levels with elevated serum unesterified fatty acids. Additionally, this mouse mutant was more susceptible to high fat diet-induced impairments in fatty acid metabolism. Quantitative reverse transcription-PCR analysis revealed that the expression of peroxisome proliferator-activated receptor γ-regulated marker genes related to adipogenesis was elevated in visceral adipose tissues. Thus, our study identifies CMO1 as the key enzyme for vitamin A production and provides evidence for a role of carotenoids as more general regulators of lipid metabolism.

scholarly journals Night Blindness and Vitamin A Deficiency following Jejunoilieal Bypass Surgery

1989 ◽  
Vol 3 (4) ◽  
pp. 138-140
Author(s):  
Paul C. Adams ◽  
Christopher L. Canny
Keyword(s):  
Vitamin A ◽  
Night Blindness ◽  
Bypass Surgery ◽  
Vitamin A Deficiency ◽  
Serum Vitamin ◽  
Jejunoileal Bypass ◽  
Intestinal Bypass ◽  
Oral Vitamin ◽  
Visual Deficits ◽  
Nutritional Vitamin

A 42-year-old man who developed severe night blindness 15 years following jejunoileal bypass surgery for morbid obesity is described. Ophthamological testing, including dark adaptation, electroretinography and serum vitamin A levels, confirmed a diagnosis of vitamin A deficiency. Oral vitamin A 25,000 iu/day for two months resulted in a full recovery of visual deficits. Nutritional vitamin A deficiency is discussed in the context of intestinal bypass surgery.

scholarly journals Effects of Chronic Hypervitaminosis a on Global Plasma Metabolome Changes and Liver Gene Expression (OR05-06-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Georg Lietz ◽  
Anthony Oxley ◽  
Kieran Finney ◽  
Adam Clark ◽  
Tim Giles ◽  
...  
Keyword(s):  
Gene Expression ◽  
Lipid Metabolism ◽  
Vitamin A ◽  
Membrane Lipids ◽  
Genetic Regulation ◽  
Reversed Phase ◽  
Plasma Metabolites ◽  
Hypervitaminosis A ◽  
Metabolomics Data ◽  
Gates Foundation

Abstract Objectives Concerns about inadvertent chronic excessive vitamin A (VA) intakes due to overly frequent supplementation, fortification and voluntarily fortified products have been raised. Although chronic excessive VA intake can create liver abnormalities, clinically detectable signs of VA toxicity are rare, indicating the need for early biomarkers of tissue damage induced by excessive VA intake. Methods To identify early markers of VA toxicity, we induced chronic hypervitaminosis A in pigs (64 pigs, 8 per group) dosed with an oral supplement of retinyl propionate (0 up to 10,000 µg/KgBW) for 17 weeks. To assess the regulatory role of vitamin A in liver metabolism, a microarray analysis was performed to identify genetic regulation in liver tissue. Gene expression data were confirmed using qRT-PCR, and differentially expressed transcripts and pathways were identified using Genespring and Ingenuity Pathway Analysis (IPA). Additionally, two untargeted UPLC-MS assays (HILIC and C18 reversed phase) were applied to analyse plasma metabolites followed by univariate and multivariate analysis. Results Metabolomics analysis indicated that between 228 to 949 plasma metabolites were statistically significant between VA treated and control animals. The majority of metabolic changes observed in plasma were lipids, with ceramides, glycerophospholipids, lysoglycerophospholipids, sterol lipids and triacylglycerides enriched in both low and high VA dosed animals. Gene expression analysis confirmed significant changes in lipid metabolism, with pathways in metabolism of terpenoids and membrane lipids significantly increased by 2.4 fold. Conclusions The combined analysis of gene expression with untargeted metabolomics data confirm that changes in liver function and lipid metabolism offers an opportunity to develop a biomarker panel to diagnose pre-symptomatic hypervitaminosis A in humans. Funding Sources Supported by the Bill and Melinda Gates foundation.

scholarly journals Increased Risk of High Body Fat and Altered Lipid Metabolism Associated to Suboptimal Consumption of Vitamin A Is Modulated by Genetic Variants rs5888 (SCARB1), rs1800629 (UCP1) and rs659366 (UCP2)

Nutrients ◽  
2020 ◽  
Vol 12 (9) ◽  
pp. 2588
Author(s):  
Sebastià Galmés ◽  
Andreu Palou ◽  
Francisca Serra
Keyword(s):  
Gene Expression ◽  
Lipid Metabolism ◽  
Vitamin A ◽  
Body Fat ◽  
Genetic Variants ◽  
Mononuclear Cells ◽  
Metabolic Response ◽  
Ex Vivo ◽  
P Value ◽  
Increased Risk

Obesity is characterized by an excessive body fat percentage (BF%). Animal and cell studies have shown benefits of vitamin A (VA) on BF% and lipid metabolism, but it is still controversial in humans. Furthermore, although some genetic variants may explain heterogeneity in VA plasma levels, their role in VA metabolic response is still scarcely characterized. This study was designed as a combination of an observational study involving 158 male subjects followed by a study with a well-balanced genotype–phenotype protocol, including in the design an ex vivo intervention study performed on isolated peripheral blood mononuclear cells (PBMCs) of the 41 former males. This is a strategy to accurately identify the delivery of Precision Nutrition recommendations to targeted subjects. The study assesses the influence of rs5888 (SCARB1), rs659366 (UCP2), and rs1800629 (UCP1) variants on higher BF% associated with suboptimal VA consumption and underlines the cellular mechanisms involved by analyzing basal and retinoic acid (RA) response on PBMC gene expression. Data show that male carriers with the major allele combinations and following suboptimal-VA diet show higher BF% (adjusted ANOVA test p-value = 0.006). Genotype–BF% interaction is observed on oxidative/inflammatory gene expression and also influences lipid related gene expression in response to RA. Data indicate that under suboptimal consumption of VA, carriers of VA responsive variants and with high-BF% show a gene expression profile consistent with an impaired basal metabolic state. The results show the relevance of consuming VA within the required amounts, its impact on metabolism and energy balance, and consequently, on men’s adiposity with a clear influence of genetic variants SCARB1, UCP2 and UCP1.

Alterations in the Lipid Metabolism of Rat Aorta: Effects of Vitamin A Deficiency

2006 ◽  
Vol 43 (6) ◽  
pp. 602-610 ◽  
Author(s):  
Laura V. Gatica ◽  
Verónica A. Vega ◽  
Fanny Zirulnik ◽  
Liliana B. Oliveros ◽  
María S. Gimenez
Keyword(s):  
Lipid Metabolism ◽  
Vitamin A ◽  
Vitamin A Deficiency ◽  
Rat Aorta

Vitamin a deficiency modifies antioxidant defenses and essential element contents in rat heart

2000 ◽  
Vol 20 (8) ◽  
pp. 1139-1150 ◽  
Author(s):  
Liliana Oliveros ◽  
Verónica Vega ◽  
Ana Cecilia Anzulovich ◽  
Darío Ramirez ◽  
María Sofia Giménez
Keyword(s):  
Vitamin A ◽  
Rat Heart ◽  
Vitamin A Deficiency ◽  
Essential Element ◽  
Antioxidant Defenses ◽  
Element Contents

Nutritional vitamin A deficiency alters antioxidant defenses and modifies the liver histoarchitecture in rat

2000 ◽  
Vol 13 (4) ◽  
pp. 343-357 ◽  
Author(s):  
Ana Cecilia Anzulovich ◽  
Liliana Beatriz Oliveros ◽  
Estela Mu�oz ◽  
Luis Dante Martinez ◽  
Maria Sofia Gimenez
Keyword(s):  
Vitamin A ◽  
Vitamin A Deficiency ◽  
Antioxidant Defenses ◽  
Nutritional Vitamin
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