Maternal Supplementation with β‐Carotene During Pregnancy Disturbs Lipid Metabolism and Glucose Homoeostasis in F1 Female Mice

2019 ◽  
Vol 63 (9) ◽  
pp. 1900072 ◽  
Author(s):  
Jiaojiao Guo ◽  
Bingshui Li ◽  
Zhenghong Zuo ◽  
Meng Chen ◽  
Chonggang Wang
Keyword(s):  
Lipid Metabolism ◽  
Female Mice ◽  
Glucose Homoeostasis ◽  
Maternal Supplementation ◽  
Β Carotene

scholarly journals Effects of maternal supplementation with fully oxidised β-carotene on the reproductive performance and immune response of sows, as well as the growth performance of nursing piglets

2020 ◽  
Vol 125 (1) ◽  
pp. 62-70 ◽  
Author(s):  
Jun Chen ◽  
Jiaming Chen ◽  
Yinzhi Zhang ◽  
Yantao Lv ◽  
Hanzhen Qiao ◽  
...  
Keyword(s):  
Immune Status ◽  
Basal Diet ◽  
Perinatal Period ◽  
Litter Weight ◽  
Lactose Concentration ◽  
Biological Similarity ◽  
Maternal Supplementation ◽  
Dietary Treatments ◽  
The Impact ◽  
Β Carotene

AbstractThe present study was conducted to evaluate the impact of dietary fully oxidised β-carotene (OxBC, C40H60O15) supplementation during the perinatal period on immune status and productivity in a sow model. At day 85 of pregnancy, 150 sows were allocated to one of three dietary treatments with fifty sows per treatment. The three experimental diets were supplemented with 0, 4 or 8 mg/kg OxBC in the basal diet. The feeding trial was conducted from gestation day 85 until day 21 of lactation. Dietary OxBC supplementation greatly enhanced colostrum IgM, IgA and IgG levels, and the IgM and IgG content of 14-d milk. Dietary OxBC supplementation decreased the TNF-α and IL-8 levels in colostrum, as well as the TNF-α and IL-18 levels in 14-d milk. There was also a tendency towards an increase in the soluble CD14 level in 14-d milk. Although dietary treatments did not affect average daily feed intake nor backfat thickness loss during lactation, dietary OxBC supplementation tended to enhance litter weight and individual piglet weight at weaning. There was a trend towards increased lactose concentration in 14-d milk with increasing dietary OxBC. It is concluded that dietary supplementation with OxBC during the perinatal period enhances the lactose concentration of sow milk and the immune status of sows, which is reflected by improved cytokine status and immunoglobulin concentrations in colostrum and milk, and thus tending to increase litter weight and individual piglet weight at weaning. The results also provide a scientific nutritional reference for perinatal mothers due to the biological similarity between pigs and humans.

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.

Gut microbiota characterization and lipid metabolism disorder found in PCB77-treated female mice

Toxicology ◽  
2019 ◽  
Vol 420 ◽  
pp. 11-20 ◽  
Author(s):  
Yulang Chi ◽  
Hongou Wang ◽  
Yi Lin ◽  
Yanyang Lu ◽  
Qiansheng Huang ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Gut Microbiota ◽  
Lipid Metabolism Disorder ◽  
Female Mice ◽  
Metabolism Disorder

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

Liver composition and lipid metabolism in NZB/W F1 female mice fed dehydroisoandrosterone

1988 ◽  
Vol 962 (1) ◽  
pp. 25-36 ◽  
Author(s):  
Bonnie C. Miller ◽  
Lau Ho-Wai ◽  
Nancy E. Tyler ◽  
Gene L. Cottam
Keyword(s):  
Lipid Metabolism ◽  
Female Mice

scholarly journals DHT Causes Liver Steatosis via Transcriptional Regulation of SCAP in Lean female Mice

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A807-A807
Author(s):  
Stanley Andrisse ◽  
Jessie Myer ◽  
Dilip “Bobby” Bogle ◽  
Nicole Eregha ◽  
Taylor Lofton
Keyword(s):  
Lipid Metabolism ◽  
Protein Expression ◽  
Low Dose ◽  
De Novo ◽  
Polycystic Ovary ◽  
Liver Steatosis ◽  
De Novo Lipogenesis ◽  
Alcoholic Fatty Liver ◽  
Female Mice ◽  
Real Time Quantitative Pcr

Abstract Hyperandrogenemia (HA) and insulin resistance are hallmarks of polycystic ovary syndrome (PCOS). These hallmarks are also integral elements of non-alcoholic fatty liver disease (NALFD). Administering low dose dihydrotestosterone (DHT) induced a lean PCOS-like female mouse model. The molecular mechanism of HA-induced NAFLD has not been determined. We hypothesized that low dose DHT would interrupt hepatic lipid metabolism leading to NAFLD. We extracted white adipose tissue (WAT), liver, and skeletal muscle from control and low dose DHT female mice; and performed histological and biochemical lipid profiles, Western blot, immunoprecipitation, chromatin immunoprecipitation, and real-time quantitative PCR analyses. DHT lowered the 65 kD form of cytosolic SREBP1 in the liver and WAT compared to controls. However, DHT did not alter the levels of the active and inactive forms of SREBP2 in the liver and WAT. DHT increased SCAP protein expression and SCAP-SREBP1 binding via AR binding to intron-8 of SCAP leading to increased SCAP mRNA. FAS mRNA and protein expression was increased in liver of DHT mice. p-ACC levels were unaltered in liver but decreased in WAT. Other lipid metabolism pathways were examined in liver and WAT, but no changes were observed. Our findings suggest that DHT increased de novo lipogenic proteins resulting in increased NAFLD via regulation of SREBP1 in liver. We show that in the presence of DHT the SCAP-SREBP1 interaction is elevated leading to increased nuclear SREBP1 resulting in increased de novo lipogenesis. We propose that the mechanism of action is increased AR binding to an ARE in SCAP intron-8.

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

Maternal supplementation with vitamin A or β-carotene and cardiovascular risk factors among pre-adolescent children in rural Nepal

2010 ◽  
Vol 1 (4) ◽  
pp. 262-270 ◽  
Author(s):  
C. P. Stewart ◽  
P. Christian ◽  
J. Katz ◽  
K. J. Schulze ◽  
L. S. F. Wu ◽  
...  
Keyword(s):  
Risk Factors ◽  
Blood Pressure ◽  
Cardiovascular Risk ◽  
Vitamin A ◽  
Cardiovascular Risk Factors ◽  
Urine Specimen ◽  
Maternal Supplementation ◽  
Rural Nepal ◽  
The Impact ◽  
Β Carotene

Vitamin A plays an important role in fetal renal and cardiovascular development, yet there has been little research on its effects on cardiovascular risk factors later in childhood. To examine this question, we followed the children of women who had been participants in a cluster-randomized, double blind, placebo-controlled trial of weekly supplementation with 7000 μg retinol equivalents of preformed vitamin A or 42 mg of β-carotene from 1994 to 1997 in rural Nepal. Women received their assigned supplements before, during and after pregnancy. Over a study period of 3 years, 17,531 infants were born to women enrolled in the trial. In 2006–2008, we revisited and assessed 13,118 children aged 9–13 years to examine the impact of maternal supplementation on early biomarkers of chronic disease. Blood pressure was measured in the entire sample of children. In a subsample of 1390 children, venous blood was collected for plasma glucose, Hb1Ac and lipids and a morning urine specimen was collected to measure the ratio of microalbumin/creatinine. Detailed anthropometry was also conducted in the subsample. The mean ±s.d.systolic and diastolic blood pressure was 97.2 ± 8.2 and 64.6 ± 8.5 mm Hg, respectively, and about 5.0% had high-blood pressure (⩾120/80 mm Hg). The prevalence of microalbuminuria (⩾30 mg/g creatinine) was also low at 4.8%. There were no differences in blood pressure or the risk of microalbuminuria between supplement groups. There were also no group differences in fasting glucose, glycated hemoglobin, triglycerides or cholesterol. Maternal supplementation with vitamin A or β-carotene had no overall impact on cardiovascular risk factors in this population at pre-adolescent age in rural Nepal.

scholarly journals Cyclopamine and Rapamycin Synergistically Inhibit mTOR Signalling in Mouse Hepatocytes, Revealing an Interaction of Hedgehog and mTor Signalling in the Liver

Cells ◽  
2020 ◽  
Vol 9 (8) ◽  
pp. 1817
Author(s):  
Luise Spormann ◽  
Christiane Rennert ◽  
Erik Kolbe ◽  
Fritzi Ott ◽  
Carolin Lossius ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Energy Homeostasis ◽  
In Vitro Studies ◽  
Primary Hepatocytes ◽  
Male And Female ◽  
Atp Production ◽  
Female Mice ◽  
Oxidative Respiration ◽  
Mtor Signalling

In the liver, energy homeostasis is mainly regulated by mechanistic target of rapamycin (mTOR) signalling, which influences relevant metabolic pathways, including lipid metabolism. However, the Hedgehog (Hh) pathway is one of the newly identified drivers of hepatic lipid metabolism. Although the link between mTOR and Hh signalling was previously demonstrated in cancer development and progression, knowledge of their molecular crosstalk in healthy liver is lacking. To close this information gap, we used a transgenic mouse model, which allows hepatocyte-specific deletion of the Hh pathway, and in vitro studies to reveal interactions between Hh and mTOR signalling. The study was conducted in male and female mice to investigate sexual differences in the crosstalk of these signalling pathways. Our results reveal that the conditional Hh knockout reduces mitochondrial adenosine triphosphate (ATP) production in primary hepatocytes from female mice and inhibits autophagy in hepatocytes from both sexes. Furthermore, in vitro studies show a synergistic effect of cyclopamine and rapamycin on the inhibition of mTor signalling and oxidative respiration in primary hepatocytes from male and female C57BL/6N mice. Overall, our results demonstrate that the impairment of Hh signalling influences mTOR signalling and therefore represses oxidative phosphorylation and autophagy.

Sign in / Sign up

Export Citation Format

Share Document