Effect of a long low-power γ-irradiation and β-carotene on lipid metabolism in the rat thymocyte nuclei

1998 ◽  
Vol 126 (3) ◽  
pp. 918-920
Author(s):  
T. P. Kulagina ◽  
S. A. Shuruta ◽  
I. K. Kolomiitseva ◽  
L. A. Vakulova
Keyword(s):  
Lipid Metabolism ◽  
Low Power ◽  
Γ Irradiation ◽  
Β Carotene

Effect of chronic γ-irradiation and β-carotene on lipid metabolism in presynaptic membranes in rat brain

2000 ◽  
Vol 129 (6) ◽  
pp. 533-536
Author(s):  
I. K. Kolomiitseva ◽  
N. I. Potekhina ◽  
T. P. Semenova ◽  
N. I. Medvinskaya ◽  
V. I. Popov ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Rat Brain ◽  
Γ Irradiation ◽  
Β Carotene

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 Tissue- and sex-specific effects of β-carotene 15,15′ oxygenase (BCO1) on retinoid and lipid metabolism in adult and developing mice

2015 ◽  
Vol 572 ◽  
pp. 11-18 ◽  
Author(s):  
Youn-Kyung Kim ◽  
Michael V. Zuccaro ◽  
Brianna K. Costabile ◽  
Rebeka Rodas ◽  
Loredana Quadro
Keyword(s):  
Lipid Metabolism ◽  
Specific Effects ◽  
Β Carotene ◽  
Developing Mice

Protection of Spermatogenesis with β-Carotene in Radiation Exposure. Message 1: Single Acute External γ-Irradiation. Short-Term Application of Carothynoid

2018 ◽  
pp. 5-14 ◽  
Author(s):  
И. Беляев ◽  
I. Belyaev ◽  
А. Самойлов ◽  
A. Samoylov
Keyword(s):  
Gamma Irradiation ◽  
Reproductive Function ◽  
Risk Groups ◽  
Drug Prevention ◽  
Embryonic Mortality ◽  
Radiation Injuries ◽  
Short Term ◽  
Γ Irradiation ◽  
Radiation Induced ◽  
Β Carotene

Purpose: Experimental evaluation of β-carotene correction of radiation induced by single acute γ-irradiation of spermatogenesis disorders in male (♂) F1 CBAxC97Bl mice and non-linear rats with short-term carotenoid prescription. Material and methods: Single external gamma irradiation ♂ was performed at the IGUR facility (137Cs, dose rate 0.029 Gy/s). The β-carotene suspension was administered ♂ orally 19 and 4 hours before, 4 and 24 hours after irradiation. The damage and effectiveness of protection of spermatogenesis of irradiated ♂ were judged by the state of their reproductive function. Results: The effects of correction of the short-term prescription of β-carotene radiation-induced by a single acute external gamma irradiation at doses of 3 and 5 Gy of spermatogenesis disorders in mice and rats at stages of mature spermatozoa, spermatids and spermatogonium have been established. β-carotene in ♂ mice reduced total embryonic mortality in 8–14 and 77–84 days after irradiation at a dose of 3 Gy from 46 to 36 and from 41 to 28 %, preimplantation – after 8–14 and 15–21 days – from 24 up to 13 and from 31 to 22 %, postimplantation – after 0–7 and 77–84 days – from 24 to 15 and from 25 to 7 %. In ♂ rats 0–7 days after irradiation at a dose of 5 Gy β-carotene reduced total, pre-, post- and induced postimplantation embryonic mortality from 62 to 41, from 34 to 17, from 41 to 30 and from 38 to 26 %, respectively. After 13–20 days – preimplantation mortality from 27 to 11 %. At the stage of spermatozoa after irradiation at a dose of 3 Gy increased the breeding efficiency from 70 to 100 %, fecundity – by 23–31 %; reduced total and preimplantation mortality from 49 to 39 % and from 41 to 27 %, respectively. At the stage of spermatids –sterilization was prevented and the efficiency of breeding was normalized, reduced post- and induced postimplantation mortality from 25 to 20 and from 17 to 12 %, respectively. The therapeutic and prophylactic effects of β-carotene at the spermatocyte stage are not revealed. In the spermatogonium stage, the carotenoid increased the total number and number of live embryos in pregnant female (♀) from 36 to 55 and from 20 to 50 %, reduced total and pre-implantation mortality from 81 to 56 and from 69 to 42 %, respectively. Conclusions: The prospects of β-carotene use for correction of gonadal radiation injuries in the risk groups of exposure to ionizing radiation and the inclusion of β-carotene in the scheme of drug prevention of acute radiation injuries of spermatogenesis are shown.

The effect of dietary supplementation of β-carotene on lipid metabolism in streptozotocin-induced diabetic rats

2004 ◽  
Vol 24 (12) ◽  
pp. 1011-1021 ◽  
Author(s):  
Jung Sook Seo ◽  
Kyeung Soon Lee ◽  
Jung Hyun Jang ◽  
Zhejiu Quan ◽  
Kyung Mi Yang ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Dietary Supplementation ◽  
Diabetic Rats ◽  
Β Carotene

scholarly journals Cardiac dysfunction in β-carotene-15,15′-dioxygenase-deficient mice is associated with altered retinoid and lipid metabolism

2014 ◽  
Vol 307 (11) ◽  
pp. H1675-H1684 ◽  
Author(s):  
Seung-Ah Lee ◽  
Hongfeng Jiang ◽  
Chad M. Trent ◽  
Jason J. Yuen ◽  
Sureshbabu Narayanasamy ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Heart Development ◽  
Fatty Acid Synthase ◽  
Hormone Receptors ◽  
Heart Function ◽  
The Body ◽  
Retinol Binding Protein ◽  
Heart Metabolism ◽  
Nonesterified Fatty Acids ◽  
Β Carotene

Dietary carotenoids like β-carotene are converted within the body either to retinoid, via β-carotene-15,15′-dioxygenase (BCO1), or to β-apo-carotenoids, via β-carotene-9′,10′-oxygenase 2. Some β-apo-carotenoids are potent antagonists of retinoic acid receptor (RAR)-mediated transcriptional regulation, which is required to ensure normal heart development and functions. We established liquid chromatography tandem mass spectrometery methods for measuring concentrations of 10 β-apo-carotenoids in mouse plasma, liver, and heart and assessed how these are influenced by Bco1 deficiency and β-carotene intake. Surprisingly, Bco1−/− mice had an increase in heart levels of retinol, nonesterified fatty acids, and ceramides and a decrease in heart triglycerides. These lipid changes were 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-γ, lipoprotein lipase, Cd36, stearoyl-CoA desaturase 1, and fatty acid synthase. We also obtained evidence of compromised heart function, as assessed by two-dimensional echocardiography, in Bco1−/− mice. However, the total absence of Bco1 did not substantially affect β-apo-carotenoid concentrations in the heart. β-Carotene administration to matched Bco1−/− and wild-type mice elevated total β-apo-carotenal levels in the heart, liver, and plasma and total β-apo-carotenoic acid levels in the liver. Thus, BCO1 modulates heart metabolism and function, possibly by altering levels of cofactors required for the actions of nuclear hormone receptors.

Production of β‐carotene in Saccharomyces cerevisiae through altering yeast lipid metabolism

2021 ◽  
Vol 118 (5) ◽  
pp. 2043-2052
Author(s):  
Yijin Zhao ◽  
Yueping Zhang ◽  
Jens Nielsen ◽  
Zihe Liu
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Lipid Metabolism ◽  
Β Carotene ◽  
Yeast Lipid

Effect of β-carotene supplementation on the expression of lipid metabolism-related genes and the deposition of back fat in beef cattle

2017 ◽  
Vol 57 (3) ◽  
pp. 513 ◽  
Author(s):  
Q. Jin ◽  
H. B. Zhao ◽  
X. M. Liu ◽  
F. C. Wan ◽  
Y. F. Liu ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Beef Cattle ◽  
Fatty Acid Synthase ◽  
Average Daily Gain ◽  
Control Level ◽  
Supplementation Period ◽  
Fat Thickness ◽  
Fat Synthesis ◽  
Fat Hydrolysis ◽  
Β Carotene

To evaluate the effects of β-carotene (βC) supplementation on lipid metabolism in the back fat of beef cattle, 120 continental crossbred (Simmental × local Luxi yellow cattle) steers were selected randomly from feedlots and allotted to four groups. Each steer was supplemented with 0, 600, 1200, or 1800 mg/day of βC for 90 days, and then received no βC for 60 days (depletion period). The βC levels significantly increased in steers supplemented with βC (P < 0.01), and then decreased to the control level by Day 150. Back fat thickness decreased slightly with increasing βC supplementation, and significantly differed among groups after supplementation ceased (P < 0.01 on Day 120, P < 0.05 on Day 150). Significant regression relationships between βC supplement level and both βC content in back fat tissue on Day 90 and back fat thickness on Days 90, 120, and 150 were established (P < 0.01). No significant differences in the dry matter intake or average daily gain were detected, but higher net meat percentages were observed in the 1200 and 1800 mg/day βC-supplemented groups compared with the control (P < 0.05). The mRNA expression of two fat synthesis-related genes, acetyl-CoA carboxylase and fatty acid synthase, were downregulated during the supplementation period, but upregulated during the next 60 days when the steers received no βC supplementation. In contrast, the expression of two fat hydrolysis-related genes, hormone-sensitive lipase and adipose triglyceride lipase, were upregulated during the supplementation period and downregulated in the subsequent 60 days. The results showed that βC supplementation suppresses back fat deposition in beef cattle by inhibiting fat synthesis and enhancing fat hydrolysis.

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