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malfunction
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a polymorphism at the beta,beta-carotene 15,15'-monooxygenase 1 (BCMO1) locus affects the response to dietary beta-carotene. Vitamin A and vitamin E status are affected by genotype or the incorporation of beta-carotene in the diet, but the effects varies according to the tissue, phenotypes, overview
malfunction
cardiac dysfunction in beta-carotene-15,15-dioxygenase-deficient mice is associated with altered retinoid and lipid metabolism. Bco1-/- mice show an increase in heart levels of retinol, nonesterified fatty acids, and ceramides and a decrease in heart triglycerides. These lipid changes are accompanied by elevations in levels of genes important to retinoid metabolism, specifically retinol dehydrogenase 10 and retinol-binding protein 4, as well as genes involved in lipid metabolism, including peroxisome proliferator-activated receptor-gamma, lipoprotein lipase, Cd36, stearoyl-CoA desaturase 1, and fatty acid synthase. The mutant mice show compromised heart function. But the total absence of Bco1 does not substantially affect beta-apo-carotenoid concentrations in the heart. Phenotype, overview
malfunction
deficiency of BCO1 in the liver does not significantly affect retinol or retinyl ester concentrations compared to the wild-type group, even though retinyl ester levels tend to be lower in the absence of BCO1. BCO1-/- and wild-type female mice reveal a statistically significant decrease in retinol content in the heart, pancreas, spleen, eye and adipose tissue of the knockout females. Retinol concentrations are greater in the lungs of the BCO1-/- females compared to wild-type
malfunction
mice lacking beta-carotene-15,15'-dioxygenase exhibit reduced serum testosterone, prostatic androgen receptor signaling, and prostatic cellular proliferation. Bco1 disruption also impacts diverse physiological end points independent of dietary carotenoid feeding, including expression of genes controlling androgen metabolism. co1 disruption significantly reduced Leydig cell number and decreased testicular mRNA expression of Hsd17b3, suggesting inhibition of testicular testosterone synthesis. Decreased androgen receptor nuclear localization in the dorsolateral prostate lobes of Bco1-/- mice. Analysis of prostatic morphology suggests a decreases in gland size and secretion, supported by reduced expression of the proliferation marker Ki-67 in Bco1-/- prostates. Genes differentially regulated in prostates of Bco1?/? mice, overview. Bco1 disruption alters prostatic morphology, reduces prostatic androgen receptor localization, and alters prostatic androgen signaling, but does not impact androgen receptor expression
malfunction
placental expression of BCMO1 and BCMO2 is altered in nitrofen-exposed rat fetuses with congenital diaphragmatic hernia, CDH. Pulmonary hypoplasia and congenital diaphragmatic hernia pathogenesis involve low pulmonary retinol levels and disrupted retinoid signaling pathway. Markedly increased decidual Bcmo1,2 immunoreactivity is observed in placental CDH group compared to controls, although not in pulmonary and liver immunoreactivity
malfunction
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placental expression of BCMO1 and BCMO2 is altered in nitrofen-exposed rat fetuses with congenital diaphragmatic hernia, CDH. Pulmonary hypoplasia and congenital diaphragmatic hernia pathogenesis involve low pulmonary retinol levels and disrupted retinoid signaling pathway. Markedly increased decidual Bcmo1,2 immunoreactivity is observed in placental CDH group compared to controls, although not in pulmonary and liver immunoreactivity
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malfunction
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deficiency of BCO1 in the liver does not significantly affect retinol or retinyl ester concentrations compared to the wild-type group, even though retinyl ester levels tend to be lower in the absence of BCO1. BCO1-/- and wild-type female mice reveal a statistically significant decrease in retinol content in the heart, pancreas, spleen, eye and adipose tissue of the knockout females. Retinol concentrations are greater in the lungs of the BCO1-/- females compared to wild-type
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malfunction
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mice lacking beta-carotene-15,15'-dioxygenase exhibit reduced serum testosterone, prostatic androgen receptor signaling, and prostatic cellular proliferation. Bco1 disruption also impacts diverse physiological end points independent of dietary carotenoid feeding, including expression of genes controlling androgen metabolism. co1 disruption significantly reduced Leydig cell number and decreased testicular mRNA expression of Hsd17b3, suggesting inhibition of testicular testosterone synthesis. Decreased androgen receptor nuclear localization in the dorsolateral prostate lobes of Bco1-/- mice. Analysis of prostatic morphology suggests a decreases in gland size and secretion, supported by reduced expression of the proliferation marker Ki-67 in Bco1-/- prostates. Genes differentially regulated in prostates of Bco1?/? mice, overview. Bco1 disruption alters prostatic morphology, reduces prostatic androgen receptor localization, and alters prostatic androgen signaling, but does not impact androgen receptor expression
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metabolism
the major fraction of retinol (recovered as retinyl esters) and carotinoids are packed into chylomicrons, which are released into the lymphocytic circulation
metabolism
the enzyme is responsible for the conversion of provitamin A carotenoids to vitamin A
metabolism
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the major fraction of retinol (recovered as retinyl esters) and carotinoids are packed into chylomicrons, which are released into the lymphocytic circulation
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physiological function
crucial enzyme in development and metabolism that governs the de novo entry of vitamin A from plant-derived precursors
physiological function
after absorption by the intestinal epithelial cells, a portion of the beta-carotene is cleaved to retinal by enzyme BCMO, which is the major beta-carotene-metabolizing enzyme and has a critical role in maintaining retinol levels
physiological function
BCO1 catalyzes central cleavage of provitamin A carotenoids at 15,15' double bond to form two molecules of all-trans-retinal which can be further metabolized to vitamin A and its derivatives
physiological function
beta-carotene-15,15'-dioxygenase (BCO1) cleaves dietary carotenoids at the central 15,15' double bond, most notably acting on beta-carotene to yield retinal
physiological function
competitive regulation of human intestinal beta-carotene 15,15'-monooxygenase 1 (BCMO1) gene expression by hepatocyte nuclear factor (HNF)-1alpha and HNF-4alpha, which are liver-enriched transcription factors that are also expressed in the small intestine, overview
physiological function
dietary carotenoids like beta-carotene are converted within the body either to retinoid, via beta-carotene-15,15'-dioxygenase (BCO1), or to beta-apo-carotenoids, via beta-carotene-9',10'-oxygenase 2. Some beta-apo-carotenoids are potent antagonists of retinoic acid receptor (RAR)-mediated transcriptional regulation, which is required to ensure normal heart development and functions. BCO1 modulates heart metabolism and function, possibly by altering levels of cofactors required for the actions of nuclear hormone receptors
physiological function
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enzyme BCMO1 is responsible for the symmetrical cleavage of beta-carotene into retinal
physiological function
retinoids are essential for fetal and lung development. Beta-carotene (BC) is the main dietary retinoid source and beta-carotene-15,15'-oxygenase-1 and 2 (Bcmo1,2) is the primary enzyme generating retinoid from BC in adult mammalian tissues. Placenta has a major role in the retinol homeostasis in fetal life: Since there is no fetal retinol synthesis, maternal retinol has to cross the placenta. The placental BCMO1 and 2 expression is tightly controlled by placental retinol level and the maternal ROH status controls fetal uptake of intact beta-carotene
physiological function
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retinoids are essential for fetal and lung development. Beta-carotene (BC) is the main dietary retinoid source and beta-carotene-15,15'-oxygenase-1 and 2 (Bcmo1,2) is the primary enzyme generating retinoid from BC in adult mammalian tissues. Placenta has a major role in the retinol homeostasis in fetal life: Since there is no fetal retinol synthesis, maternal retinol has to cross the placenta. The placental BCMO1 and 2 expression is tightly controlled by placental retinol level and the maternal ROH status controls fetal uptake of intact beta-carotene
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physiological function
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after absorption by the intestinal epithelial cells, a portion of the beta-carotene is cleaved to retinal by enzyme BCMO, which is the major beta-carotene-metabolizing enzyme and has a critical role in maintaining retinol levels
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physiological function
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beta-carotene-15,15'-dioxygenase (BCO1) cleaves dietary carotenoids at the central 15,15' double bond, most notably acting on beta-carotene to yield retinal
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