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Referências encontradas : 114 [refinar]
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[PMID]:28549616
[Au] Autor:Zhu RG; Sun YD; Hou YT; Fan JG; Chen G; Li TP
[Ad] Endereço:Department of Food Science, College of Light Industry, Liaoning University, Liaoning Engineering Research Center for Food Bioprocessing, Shenyang Key Laboratory of Food Bioprocessing and Quality Control, Shenyang 110036, China. Electronic address: zhurugang@lnu.edu.cn.
[Ti] Título:Pectin penta-oligogalacturonide reduces cholesterol accumulation by promoting bile acid biosynthesis and excretion in high-cholesterol-fed mice.
[So] Source:Chem Biol Interact;272:153-159, 2017 Jun 25.
[Is] ISSN:1872-7786
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Haw pectin penta-oligogalacturonide (HPPS) has important role in improving cholesterol metabolism and promoting the conversion of cholesterol to bile acids (BA) in mice fed high-cholesterol diet (HCD). However, the mechanism is not clear. This study aims to investigate the effects of HPPS on cholesterol accumulation and the regulation of hepatic BA synthesis and transport in HCD-fed mice. Results showed that HPPS significantly decreased plasma and hepatic TC levels but increased plasma high-density lipoprotein cholesterol (HDL-C) and apolipoprotein A-I (apoA-I) levels, compared to HCD. BA analysis showed that HPPS markedly decreased hepatic and small intestine BA levels but increased the gallbladder BA levels, and finally decreased the total BA pool size, compared to HCD. Studies of molecular mechanism revealed that HPPS promoted hepatic ATP-binding cassette transporter A1 (ABCA1), ATP-binding cassette transporter G1 (ABCG1), and scavenger receptor BI (SR-BI) expression but did not affect ATB binding cassette transporter G5/G8 (ABCG5/8) expression. HPPS inactivated hepatic farnesoid X receptor (FXR) and target genes expression, which resulted in significant increase of cholesterol 7α-hydroxylase 1 (CYP7A1) and sterol 12α-hydroxylase (CYP8B1) expression, with up-regulations of 204.2% and 33.5% for mRNA levels, respectively, compared with HCD. In addition, HPPS markedly enhanced bile salt export pump (BSEP) expression but didn't affect the sodium/taurocholate co-transporting polypeptide (NTCP) expression. In conclusion, the study revealed that HPPS reduced cholesterol accumulation by promoting BA synthesis in the liver and excretion in the feces, and might promote macrophage-to-liver reverse cholesterol transport (RCT) but did not liver-to-fecal RCT.
[Mh] Termos MeSH primário: Ácidos e Sais Biliares/metabolismo
Colesterol/sangue
Expressão Gênica/efeitos dos fármacos
Oligossacarídeos/farmacologia
Pectinas/farmacologia
[Mh] Termos MeSH secundário: Transportador 1 de Cassete de Ligação de ATP/genética
Transportador 1 de Cassete de Ligação de ATP/metabolismo
Membro 1 da Subfamília G de Transportadores de Cassetes de Ligação de ATP/genética
Membro 1 da Subfamília G de Transportadores de Cassetes de Ligação de ATP/metabolismo
Animais
Apolipoproteína A-I/sangue
Colesterol 7-alfa-Hidroxilase/genética
Colesterol 7-alfa-Hidroxilase/metabolismo
HDL-Colesterol/sangue
Dieta Hiperlipídica
Intestino Delgado/efeitos dos fármacos
Intestino Delgado/metabolismo
Fígado/efeitos dos fármacos
Fígado/metabolismo
Masculino
Camundongos
Pectinas/química
Receptores Depuradores Classe B/genética
Receptores Depuradores Classe B/metabolismo
Esteroide 12-alfa-Hidroxilase/genética
Esteroide 12-alfa-Hidroxilase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ABCA1 protein, mouse); 0 (ABCG1 protein, mouse); 0 (ATP Binding Cassette Transporter 1); 0 (ATP Binding Cassette Transporter, Sub-Family G, Member 1); 0 (Apolipoprotein A-I); 0 (Bile Acids and Salts); 0 (Cholesterol, HDL); 0 (Oligosaccharides); 0 (Pectins); 0 (Scarb1 protein, mouse); 0 (Scavenger Receptors, Class B); 97C5T2UQ7J (Cholesterol); EC 1.14.14.23 (Cholesterol 7-alpha-Hydroxylase); EC 1.14.14.23 (Cyp7a1 protein, mouse); EC 1.14.18.8 (Steroid 12-alpha-Hydroxylase)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170620
[Lr] Data última revisão:
170620
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170528
[St] Status:MEDLINE


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[PMID]:28377401
[Au] Autor:Bertaggia E; Jensen KK; Castro-Perez J; Xu Y; Di Paolo G; Chan RB; Wang L; Haeusler RA
[Ad] Endereço:Department of Pathology and Cell Biology, Columbia University, New York, New York.
[Ti] Título: ablation prevents Western diet-induced weight gain and hepatic steatosis because of impaired fat absorption.
[So] Source:Am J Physiol Endocrinol Metab;313(2):E121-E133, 2017 Aug 01.
[Is] ISSN:1522-1555
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Bile acids (BAs) are cholesterol derivatives that regulate lipid metabolism, through their dual abilities to promote lipid absorption and activate BA receptors. However, different BA species have varying abilities to perform these functions. Eliminating 12α-hydroxy BAs in mice via knockout causes low body weight and improved glucose tolerance. The goal of this study was to determine mechanisms of low body weight in mice. We challenged mice with a Western-type diet and assessed body weight and composition. We measured energy expenditure, fecal calories, and lipid absorption and performed lipidomic studies on feces and intestine. We investigated the requirement for dietary fat in the phenotype using a fat-free diet. mice were resistant to Western diet-induced body weight gain, hepatic steatosis, and insulin resistance. These changes were associated with increased fecal calories, due to malabsorption of hydrolyzed dietary triglycerides. This was reversed by treating the mice with taurocholic acid, the major 12α-hydroxylated BA species. The improvements in body weight and steatosis were normalized by feeding mice a fat-free diet. The effects of BA composition on intestinal lipid handling are important for whole body energy homeostasis. Thus modulating BA composition is a potential tool for obesity or diabetes therapy.
[Mh] Termos MeSH primário: Dieta Ocidental/efeitos adversos
Gorduras na Dieta/metabolismo
Fígado Gorduroso/genética
Absorção Intestinal/genética
Metabolismo dos Lipídeos/genética
Esteroide 12-alfa-Hidroxilase/genética
Ganho de Peso/genética
[Mh] Termos MeSH secundário: Animais
Ácidos e Sais Biliares/metabolismo
Dieta Hiperlipídica
Fígado Gorduroso/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bile Acids and Salts); 0 (Dietary Fats); EC 1.14.18.8 (Steroid 12-alpha-Hydroxylase)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170907
[Lr] Data última revisão:
170907
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170406
[St] Status:MEDLINE
[do] DOI:10.1152/ajpendo.00409.2016


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[PMID]:28120707
[Au] Autor:Moris D; Giaginis C; Tsourouflis G; Theocharis S
[Ad] Endereço:First Department of Pathology, Medical School, National and Kapodistrian University of Athens, Athens. Greece.
[Ti] Título:Farnesoid-X Receptor (FXR) as a Promising Pharmaceutical Target in Atherosclerosis.
[So] Source:Curr Med Chem;24(11):1147-1157, 2017 May 31.
[Is] ISSN:1875-533X
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Atherosclerosis (AS) is a major cause of death and morbidity in Western world and is strongly connected with atherogenic lipoproteins and inflammation. Bile acids (BA) act as activating signals of endogenous ligands such as Farnesoid-X receptor (FXR). Primary data indicate a potential role of FXR in AS. The therapeutic value of FXR ligands in AS is unknown. OBJECTIVE: With the present review, we analyzed the efficacy of FXR agonists as a therapeutic modalities against AS. In this aspect, we performed an electronic search through Pub- Med/MEDLINE database by using the key terms: FXR*, Farnesoid X receptor*, atherosclerosis*, bile acids* and agonism*. CONCLUSION: According to our analysis, the FXR seems to be a promising therapeutic target in the atherosclerosis natural history. FXR agonism could exert protective effects in the development and evolution of AS. However, concomitant side effects such as the reduction of plasma HDL have been reported. Finally, results from undergoing clinical trials with synthetic FXR agonists will shed more light to the precise role of FXR agonism in AS treatment.
[Mh] Termos MeSH primário: Aterosclerose/patologia
Receptores Citoplasmáticos e Nucleares/metabolismo
[Mh] Termos MeSH secundário: Animais
Aterosclerose/tratamento farmacológico
Aterosclerose/metabolismo
Ácidos e Sais Biliares/metabolismo
Ácidos e Sais Biliares/farmacologia
Ácidos e Sais Biliares/uso terapêutico
Colesterol 7-alfa-Hidroxilase/genética
Colesterol 7-alfa-Hidroxilase/metabolismo
Seres Humanos
Receptores Citoplasmáticos e Nucleares/agonistas
Receptores Citoplasmáticos e Nucleares/genética
Esteroide 12-alfa-Hidroxilase/genética
Esteroide 12-alfa-Hidroxilase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (6-ethyl-24-norcholane-3,7,23-triol-23 sulfate); 0 (Bile Acids and Salts); 0 (Receptors, Cytoplasmic and Nuclear); 0 (farnesoid X-activated receptor); EC 1.14.14.23 (Cholesterol 7-alpha-Hydroxylase); EC 1.14.18.8 (Steroid 12-alpha-Hydroxylase)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170908
[Lr] Data última revisão:
170908
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170126
[St] Status:MEDLINE
[do] DOI:10.2174/0929867324666170124151940


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[PMID]:26511794
[Au] Autor:McGavigan AK; Garibay D; Henseler ZM; Chen J; Bettaieb A; Haj FG; Ley RE; Chouinard ML; Cummings BP
[Ad] Endereço:Department of Biomedical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, New York, USA.
[Ti] Título:TGR5 contributes to glucoregulatory improvements after vertical sleeve gastrectomy in mice.
[So] Source:Gut;66(2):226-234, 2017 Feb.
[Is] ISSN:1468-3288
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Vertical sleeve gastrectomy (VSG) produces high rates of type 2 diabetes remission; however, the mechanisms responsible remain incompletely defined. VSG increases circulating bile acid concentrations and bile acid signalling through TGR5 improves glucose homeostasis. Therefore, we investigated the role of TGR5 signalling in mediating the glucoregulatory benefits of VSG. DESIGN: VSG or sham surgery was performed in high-fat-fed male Tgr5 (wild type) and Tgr5 (knockout) littermates. Sham-operated mice were fed ad libitum or food restricted to match their body weight to VSG-operated mice. Body weight, food intake, energy expenditure, insulin signalling and circulating bile acid profiles were measured and oral glucose tolerance testing, islet immunohistochemistry and gut microbial profiling were performed. RESULTS: VSG decreased food intake and body weight, increased energy expenditure and circulating bile acid concentrations, improved fasting glycaemia, glucose tolerance and glucose-stimulated insulin secretion, enhanced nutrient-stimulated glucagon-like peptide 1 secretion and produced favourable shifts in gut microbial populations in both genotypes. However, the body weight-independent improvements in fasting glycaemia, glucose tolerance, hepatic insulin signalling, hepatic inflammation and islet morphology after VSG were attenuated in Tgr5 relative to Tgr5 mice. Furthermore, VSG produced metabolically favourable alterations in circulating bile acid profiles that were blunted in Tgr5 relative to Tgr5 mice. TGR5-dependent regulation of hepatic Cyp8b1 expression may have contributed to TGR5-mediated shifts in the circulating bile acid pool after VSG. CONCLUSIONS: These results suggest that TGR5 contributes to the glucoregulatory benefits of VSG surgery by promoting metabolically favourable shifts in the circulating bile acid pool.
[Mh] Termos MeSH primário: Ácidos e Sais Biliares/sangue
Glicemia/metabolismo
Gastrectomia
Insulina/secreção
Receptores Acoplados a Proteínas-G/metabolismo
[Mh] Termos MeSH secundário: Animais
Peso Corporal
Ingestão de Alimentos
Metabolismo Energético
Jejum
Gastrectomia/métodos
Microbioma Gastrointestinal
Peptídeo 1 Semelhante ao Glucagon/secreção
Teste de Tolerância a Glucose
Insulina/metabolismo
Ilhotas Pancreáticas/química
Ilhotas Pancreáticas/patologia
Fígado/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Receptores Acoplados a Proteínas-G/genética
Transdução de Sinais
Esteroide 12-alfa-Hidroxilase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bile Acids and Salts); 0 (Blood Glucose); 0 (Gpbar1 protein, mouse); 0 (Insulin); 0 (Receptors, G-Protein-Coupled); 89750-14-1 (Glucagon-Like Peptide 1); EC 1.14.18.8 (Steroid 12-alpha-Hydroxylase)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170719
[Lr] Data última revisão:
170719
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:151030
[St] Status:MEDLINE
[do] DOI:10.1136/gutjnl-2015-309871


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[PMID]:27832649
[Au] Autor:Yang H; Duan Z
[Ad] Endereço:The Second Department of Gastroenterology, The First Affiliated Hospital of Dalian Medical University, Dalian, China.
[Ti] Título:Bile Acids and the Potential Role in Primary Biliary Cirrhosis.
[So] Source:Digestion;94(3):145-153, 2016.
[Is] ISSN:1421-9867
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Bile acids (BAs) play a potential role in regulating the whole-body metabolic homeostasis via the interaction with gut microbiome and the signal transduction as messengers, which establish a link between the primary biliary cirrhosis (PBC) and gut microbiome in many aspects, particularly with regard to the immune system of the body. PBC, as a chronic cholestatic liver disease characterised by the destruction of small intrahepatic bile ducts, causes fibrosis and potential cirrhosis without efficient therapies. SUMMARY: Recent researches show BAs can induce the differentiation of hepatic stellate cells, suggesting that it may serve as a novel therapy to resist, even changeover the irreversible liver cirrhosis in PBC. Key Messages: In this review, we conclude and provide information on the possible mechanism of pleiotropic BAs in homeostasis of the gut microbiome and liver regeneration, and hope to broaden the therapy of PBC and promote the relevant drugs' development.
[Mh] Termos MeSH primário: Ácidos e Sais Biliares/metabolismo
Microbioma Gastrointestinal/imunologia
Cirrose Hepática Biliar/imunologia
Cirrose Hepática Biliar/metabolismo
Fígado/fisiologia
Regeneração
[Mh] Termos MeSH secundário: Ductos Biliares Intra-Hepáticos/patologia
Colesterol 7-alfa-Hidroxilase/metabolismo
Células Estreladas do Fígado/fisiologia
Hepatócitos/metabolismo
Seres Humanos
Transdução de Sinais
Esteroide 12-alfa-Hidroxilase/metabolismo
alfa Catenina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Bile Acids and Salts); 0 (alpha Catenin); EC 1.14.14.23 (CYP7A1 protein, human); EC 1.14.14.23 (Cholesterol 7-alpha-Hydroxylase); EC 1.14.18.8 (Steroid 12-alpha-Hydroxylase)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170330
[Lr] Data última revisão:
170330
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161111
[St] Status:MEDLINE
[do] DOI:10.1159/000452300


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[PMID]:27621183
[Au] Autor:Yamada A; Honma K; Mochizuki K; Goda T
[Ad] Endereço:Laboratory of Nutritional Physiology, Graduate School of Nutritional and Environmental Sciences, Laboratory of Nutritional Physiology, University of Shizuoka, Shizuoka, Japan.
[Ti] Título:BRD4 regulates fructose-inducible lipid accumulation-related genes in the mouse liver.
[So] Source:Metabolism;65(10):1478-88, 2016 Oct.
[Is] ISSN:1532-8600
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Fructose intake induces hepatic steatosis by activating fat synthesis. In this study, we searched for genes that showed acute induction in the livers of mice force-fed with fructose, and examined how this induction is regulated. MATERIALS/METHODS: We identified genes induced at 6h after the fructose force-feeding using a microarray and quantitative real-time RT-PCR. Histone acetylation and an acetylated histone binding protein bromodomain containing (BRD)4 binding around the fructose-inducible genes were examined using a chromatin immunoprecipitation assay. We examined whether (+)-JQ1, an inhibitor of the binding between the BRD4 and acetylated histones, inhibited the expressions of fructose-inducible genes, histone acetylation and BRD4 binding around the genes. RESULTS: We identified upregulated genes related to lipid accumulation, such as Cyp8b1, Dak and Plin5, in mice force-fed with fructose compared with those force-fed with glucose. Acetylation of histones H3 and H4, and BRD4 binding around the transcribed region of those fructose-inducible genes, were enhanced by fructose force-feeding. Meanwhile, (+)-JQ1 treatment reduced expressions of fructose-inducible genes, histone acetylation and BRD4 binding around these genes. CONCLUSIONS: Acute induction of genes related to lipid accumulation in the livers of mice force-fed with fructose is associated with the induction of histone acetylation and BRD4 binding around these genes.
[Mh] Termos MeSH primário: Frutose/farmacologia
Metabolismo dos Lipídeos/efeitos dos fármacos
Metabolismo dos Lipídeos/genética
Fígado/efeitos dos fármacos
Fígado/metabolismo
Proteínas Nucleares/metabolismo
Fatores de Transcrição/metabolismo
[Mh] Termos MeSH secundário: Acetilação
Animais
Regulação da Expressão Gênica/efeitos dos fármacos
Histonas/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Proteínas Nucleares/antagonistas & inibidores
Perilipina-5/metabolismo
Processamento de Proteína Pós-Traducional
Esteroide 12-alfa-Hidroxilase/metabolismo
Fatores de Transcrição/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Brd4 protein, mouse); 0 (Histones); 0 (Nuclear Proteins); 0 (Perilipin-5); 0 (Transcription Factors); 30237-26-4 (Fructose); EC 1.14.18.8 (Steroid 12-alpha-Hydroxylase)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170517
[Lr] Data última revisão:
170517
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160914
[St] Status:MEDLINE


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[PMID]:26824238
[Au] Autor:Bonde Y; Eggertsen G; Rudling M
[Ad] Endereço:Department of Medicine, Karolinska Institute, Karolinska University Hospital Huddinge, Stockholm, Sweden.
[Ti] Título:Mice Abundant in Muricholic Bile Acids Show Resistance to Dietary Induced Steatosis, Weight Gain, and to Impaired Glucose Metabolism.
[So] Source:PLoS One;11(1):e0147772, 2016.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:High endogenous production of, or treatment with muricholic bile acids, strongly reduces the absorption of cholesterol. Mice abundant in muricholic bile acids may therefore display an increased resistance against dietary induced weight gain, steatosis, and glucose intolerance due to an anticipated general reduction in lipid absorption. To test this hypothesis, mice deficient in steroid 12-alpha hydroxylase (Cyp8b1-/-) and therefore abundant in muricholic acids were monitored for 11 weeks while fed a high fat diet. Food intake and body and liver weights were determined, and lipids in liver, serum and feces were measured. Further, responses during oral glucose and intraperitoneal insulin tolerance tests were evaluated. On the high fat diet, Cyp8b1-/- mice displayed less weight gain compared to wildtype littermates (Cyp8b1+/+). In addition, liver enlargement with steatosis and increases in serum LDL-cholesterol were strongly attenuated in Cyp8b1-/- mice on high fat diet. Fecal excretion of cholesterol was increased and there was a strong trend for doubled fecal excretion of free fatty acids, while excretion of triglycerides was unaltered, indicating dampened lipid absorption. On high fat diet, Cyp8b1-/- mice also presented lower serum glucose levels in response to oral glucose gavage or to intraperitoneal insulin injection compared to Cyp8b1+/+. In conclusion, following exposure to a high fat diet, Cyp8b1-/- mice are more resistant against weight gain, steatosis, and to glucose intolerance than Cyp8b1+/+ mice. Reduced lipid absorption may in part explain these findings. Overall, the results suggest that muricholic bile acids may be beneficial against the metabolic syndrome.
[Mh] Termos MeSH primário: Ácidos Cólicos/metabolismo
Fígado Gorduroso/metabolismo
Fígado Gorduroso/patologia
Glucose/metabolismo
Fígado/patologia
[Mh] Termos MeSH secundário: Animais
Colesterol/metabolismo
Dieta Hiperlipídica/efeitos adversos
Fígado Gorduroso/genética
Feminino
Deleção de Genes
Intolerância à Glucose/genética
Intolerância à Glucose/metabolismo
Intolerância à Glucose/patologia
Fígado/metabolismo
Masculino
Camundongos
Esteroide 12-alfa-Hidroxilase/genética
Ganho de Peso
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cholic Acids); 39016-49-4 (muricholic acid); 97C5T2UQ7J (Cholesterol); EC 1.14.18.8 (Steroid 12-alpha-Hydroxylase); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:161126
[Lr] Data última revisão:
161126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160130
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0147772


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[PMID]:26388416
[Au] Autor:Oh Y; Jin Y; Park Y
[Ad] Endereço:Department of Food and Nutrition,Hanyang University,Seoul 133-791,South Korea.
[Ti] Título:Synergic hypocholesterolaemic effect of n-3 PUFA and oestrogen by modulation of hepatic cholesterol metabolism in female rats.
[So] Source:Br J Nutr;114(11):1766-73, 2015 Dec 14.
[Is] ISSN:1475-2662
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:n-3 PUFA such as EPA and DHA as well as oestrogen have been reported to decrease blood levels of cholesterol, but their underlying mechanism is unclear. The purpose of this study was to determine the effects of the combination of n-3 PUFA supplementation and oestrogen injection on hepatic cholesterol metabolism. Rats were fed a modified AIN-93G diet with 0, 1 or 2 % n-3 PUFA (EPA+DHA) relative to the total energy intake for 12 weeks. Rats were surgically ovariectomised at week 8, and, after 1-week recovery, rats were injected with 17ß-oestradiol-3-benzoate (E2) or maize oil for the last 3 weeks. Supplementation with n-3 PUFA and E2 injection significantly increased the ratio of the hepatic expression of phosphorylated AMP activated protein kinase (p-AMPK):AMP activated protein kinase (AMPK) and decreased sterol regulatory element-binding protein-2, 3-hydroxy-3-methylglutaryl coenzyme A reductase and proprotein convertase subtilisin/kexin type 9. Supplementation with n-3 PUFA increased hepatic expression of cholesterol 7α-hydroxylase (CYP7A1), sterol 12α-hydroxylase (CYP8B1) and sterol 27-hydroxylase (CYP27A1); however, E2 injection decreased CYP7A1 and CYP8B1 but not CYP27A1. Additionally, E2 injection increased hepatic expression of oestrogen receptor-α and ß. In conclusion, n-3 PUFA supplementation and E2 injection had synergic hypocholesterolaemic effects by down-regulating hepatic cholesterol synthesis (n-3 PUFA and oestrogen) and up-regulating bile acid synthesis (n-3 PUFA) in ovariectomised rats.
[Mh] Termos MeSH primário: Envelhecimento
Anticolesterolemiantes/uso terapêutico
Suplementos Nutricionais
Estrogênios/uso terapêutico
Ácidos Graxos Ômega-3/uso terapêutico
Hipercolesterolemia/prevenção & controle
Fígado/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Anticolesterolemiantes/administração & dosagem
Colestanotriol 26-Mono-Oxigenase/química
Colestanotriol 26-Mono-Oxigenase/metabolismo
Colesterol 7-alfa-Hidroxilase/química
Colesterol 7-alfa-Hidroxilase/metabolismo
Terapia Combinada
Dieta com Restrição de Gorduras
Estradiol/administração & dosagem
Estradiol/análogos & derivados
Estradiol/uso terapêutico
Estrogênios/administração & dosagem
Ácidos Graxos Ômega-3/administração & dosagem
Feminino
Hidroximetilglutaril-CoA Redutases/química
Hidroximetilglutaril-CoA Redutases/metabolismo
Hipercolesterolemia/enzimologia
Hipercolesterolemia/metabolismo
Fígado/enzimologia
Fígado/metabolismo
Ovariectomia
Pró-Proteína Convertase 9
Distribuição Aleatória
Ratos Wistar
Serina Endopeptidases/química
Serina Endopeptidases/metabolismo
Esteroide 12-alfa-Hidroxilase/química
Esteroide 12-alfa-Hidroxilase/metabolismo
Proteína de Ligação a Elemento Regulador de Esterol 2/antagonistas & inibidores
Proteína de Ligação a Elemento Regulador de Esterol 2/metabolismo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anticholesteremic Agents); 0 (Estrogens); 0 (Fatty Acids, Omega-3); 0 (Sterol Regulatory Element Binding Protein 2); 1S4CJB5ZGN (estradiol 3-benzoate); 4TI98Z838E (Estradiol); EC 1.1.1.- (Hydroxymethylglutaryl CoA Reductases); EC 1.14.14.23 (CYP7A1 protein, rat); EC 1.14.14.23 (Cholesterol 7-alpha-Hydroxylase); EC 1.14.15.15 (Cholestanetriol 26-Monooxygenase); EC 1.14.15.15 (Cyp27a1 protein, rat); EC 1.14.18.8 (Steroid 12-alpha-Hydroxylase); EC 3.4.21.- (PCSK9 protein, rat); EC 3.4.21.- (Proprotein Convertase 9); EC 3.4.21.- (Serine Endopeptidases)
[Em] Mês de entrada:1602
[Cu] Atualização por classe:161126
[Lr] Data última revisão:
161126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150922
[St] Status:MEDLINE
[do] DOI:10.1017/S0007114515003517


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[PMID]:26198044
[Au] Autor:Sharanek A; Burban A; Humbert L; Bachour-El Azzi P; Felix-Gomes N; Rainteau D; Guillouzo A
[Ad] Endereço:*INSERM U991, Foie, Métabolismes et Cancer Rennes, France; Université de Rennes 1, Rennes, France; and andre.guillouzo@univ-rennes1.fr.
[Ti] Título:Cellular Accumulation and Toxic Effects of Bile Acids in Cyclosporine A-Treated HepaRG Hepatocytes.
[So] Source:Toxicol Sci;147(2):573-87, 2015 Oct.
[Is] ISSN:1096-0929
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Alteration of bile acid (BA) profiles and secretion by cholestatic drugs represents a major clinical issue. Species differences exist in BA composition, synthesis, and regulation; however presently, there is no in vitro reproducible cell model to perform studies on BAs in humans. We have evaluated the capacity of the human HepaRG cell line to synthesize, conjugate, and secrete BAs, and analyzed changes in BA content and profile after cyclosporine A (CsA) treatment. Our data show that HepaRG cells produced normal BAs at daily levels comparable, though in different proportions, to those measured in primary human hepatocytes. A 4-h treatment with CsA led to BA accumulation and profile changes associated with occurrence of cholestatic features, while after 24 h BAs were decreased in cell layers and increased in media. The latter effects resulted from reduced function of BA uptake transporter (Na(+)-taurocholate cotransporting polypeptide), reduced expression of BA metabolizing enzymes, including cytochrome P4507A1, cytochrome P4508B1, and cytochrome P45027A1, and induction of alternative basolateral transporters. Noteworthy, HepaRG cells incubated in a 2% serum-supplemented medium showed dose-dependent accumulation of the cytotoxic BA lithocholic acid in a nonsulfoconjugated form associated with early inhibition of the canalicular transporter MRP2 and sulfotransferase 2A1. In summary, our data bring the first demonstration that an in vitro human liver cell line is able to produce and secrete conjugated BAs, and to accumulate endogenous BAs transiently, concomitantly to occurrence of various other cholestatic features following CsA treatment. Retention of the hydrophobic lithocholic acid supports its toxic role in drug-induced cholestasis. Overall, our results argue on the suitability of HepaRG cells for investigating mechanisms involved in the development of the disease.
[Mh] Termos MeSH primário: Ácidos e Sais Biliares/toxicidade
Ciclosporina/farmacologia
Hepatócitos/efeitos dos fármacos
[Mh] Termos MeSH secundário: Ácidos e Sais Biliares/análise
Ácidos e Sais Biliares/metabolismo
Western Blotting
Linhagem Celular
Colestanotriol 26-Mono-Oxigenase/metabolismo
Colesterol 7-alfa-Hidroxilase/metabolismo
Relação Dose-Resposta a Droga
Expressão Gênica/efeitos dos fármacos
Hepatócitos/química
Seres Humanos
Esteroide 12-alfa-Hidroxilase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Bile Acids and Salts); 83HN0GTJ6D (Cyclosporine); EC 1.14.14.23 (CYP7A1 protein, human); EC 1.14.14.23 (Cholesterol 7-alpha-Hydroxylase); EC 1.14.15.15 (CYP27A1 protein, human); EC 1.14.15.15 (Cholestanetriol 26-Monooxygenase); EC 1.14.18.8 (Steroid 12-alpha-Hydroxylase)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150723
[St] Status:MEDLINE
[do] DOI:10.1093/toxsci/kfv155


  10 / 114 MEDLINE  
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[PMID]:26040663
[Au] Autor:Meng Q; Chen X; Wang C; Liu Q; Sun H; Sun P; Huo X; Liu Z; Yao J; Liu K
[Ad] Endereço:Department of Clinical Pharmacology, College of Pharmacy, Dalian Medical University, 9 West Section, Lvshun South Road, Dalian, 116044, China.
[Ti] Título:Protective Effects of Alisol B 23-Acetate Via Farnesoid X Receptor-Mediated Regulation of Transporters and Enzymes in Estrogen-Induced Cholestatic Liver Injury in Mice.
[So] Source:Pharm Res;32(11):3688-98, 2015 Nov.
[Is] ISSN:1573-904X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE: To investigate protective effects of alisol B 23-acetate (AB23A) against hepatotoxity and cholestasis induced by 17α-ethinylestradiol (EE) in association with farnesoid X receptor (FXR) activation in vivo and in vitro. METHODS: The cholestatic liver injury model was established by subcutaneous injections of EE in C57BL/6 mice. Serum biomarkers, bile flow assay and H&E staining were used to identify the amelioration of cholestasis after AB23A treatment. Mice primary hepatocytes culture, gene silencing experiment, real-time PCR and Western blot assay were used to elucidate the mechanisms underlying AB23A hepatoprotection. RESULTS: AB23A treatment protected against liver injury induced by EE through increasing hepatic efflux and reducing uptake of bile acid via an induction in efflux transporters (Bsep and Mrp2) and an inhibition in hepatic uptake transporter (Ntcp) expression. AB23A also reduced bile acid synthesis through repressing Cyp7a1 and Cyp8b1, and increased bile acid metabolism through an induction in gene expression of Sult2a1. We further demonstrated that the changes in transporters and enzymes, as well as ameliorative liver histology in AB23A-treated mice were abrogated by FXR antagonist guggulsterone in vivo and were abrogated after FXR was silenced in vitro. CONCLUSIONS: AB23A produces protective effects against EE-induced cholestasis, due to FXR-mediated gene regulation.
[Mh] Termos MeSH primário: Doença Hepática Induzida por Substâncias e Drogas/enzimologia
Doença Hepática Induzida por Substâncias e Drogas/prevenção & controle
Colestase/induzido quimicamente
Colestenonas/uso terapêutico
Proteínas de Membrana Transportadoras/metabolismo
Receptores Citoplasmáticos e Nucleares/metabolismo
[Mh] Termos MeSH secundário: Membro 11 da Subfamília B de Transportadores de Cassetes de Ligação de ATP
Transportadores de Cassetes de Ligação de ATP/genética
Transportadores de Cassetes de Ligação de ATP/metabolismo
Animais
Doença Hepática Induzida por Substâncias e Drogas/patologia
Colestase/complicações
Colestase/patologia
Colestenonas/administração & dosagem
Colesterol 7-alfa-Hidroxilase/genética
Colesterol 7-alfa-Hidroxilase/metabolismo
Modelos Animais de Doenças
Etinilestradiol/toxicidade
Hepatócitos/efeitos dos fármacos
Hepatócitos/metabolismo
Testes de Função Hepática
Masculino
Proteínas de Membrana Transportadoras/genética
Camundongos Endogâmicos C57BL
Proteínas Associadas à Resistência a Múltiplos Medicamentos/genética
Proteínas Associadas à Resistência a Múltiplos Medicamentos/metabolismo
Transportadores de Ânions Orgânicos Dependentes de Sódio/genética
Transportadores de Ânions Orgânicos Dependentes de Sódio/metabolismo
Cultura Primária de Células
Esteroide 12-alfa-Hidroxilase/genética
Esteroide 12-alfa-Hidroxilase/metabolismo
Simportadores/genética
Simportadores/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (ATP Binding Cassette Subfamily B Member 11); 0 (Abcb11 protein, mouse); 0 (Cholestenones); 0 (Membrane Transport Proteins); 0 (Multidrug Resistance-Associated Proteins); 0 (Organic Anion Transporters, Sodium-Dependent); 0 (Receptors, Cytoplasmic and Nuclear); 0 (Symporters); 0 (alisol B 23-acetate); 0 (farnesoid X-activated receptor); 145420-23-1 (sodium-bile acid cotransporter); 423D2T571U (Ethinyl Estradiol); 4AF605U6JN (multidrug resistance-associated protein 2); EC 1.14.14.23 (Cholesterol 7-alpha-Hydroxylase); EC 1.14.18.8 (Steroid 12-alpha-Hydroxylase)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150605
[St] Status:MEDLINE
[do] DOI:10.1007/s11095-015-1727-x



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