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Pesquisa : D08.811.277.352.897.387.100 [Categoria DeCS]
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[PMID]:29273553
[Au] Autor:Raza SHA; Gui L; Khan R; Schreurs NM; Xiaoyu W; Wu S; Mei C; Wang L; Ma X; Wei D; Guo H; Zhang S; Wang X; Kaleri HA; Zan L
[Ad] Endereço:College of Animal Science and Technology, Northwest A&F University, Yangling, Shaanxi 712100, PR China; National Beef Cattle Improvement Center of Northwest A&F University, Yangling 712100, PR China.
[Ti] Título:Association between FASN gene polymorphisms ultrasound carcass traits and intramuscular fat in Qinchuan cattle.
[So] Source:Gene;645:55-59, 2018 Mar 01.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Fatty acid synthase (FASN) is an enzyme involved with fat deposition and fatty acid composition in cattle. This study was conducted to detect single nucleotide polymorphisms (SNPs) of the FASN gene and explore their relationships with ultrasound carcass traits in order to assess the potential use of the FASN gene for the breeding selection of Qinchuan cattle for desirable carcass traits. The frequencies of SNP g.12740C>T, g.13192T>C and g.13232C>T were identified in 525 individual Qinchuan cattle which were also assessed for backfat depth, eye muscle area and intramuscular fat by ultrasound. According to the PIC values, g.13192T>C possessed an intermediate polymorphism (0.25T, g.12740C>T possessed low polymorphism (PIC<0.25). Chi-square tests showed that g.13192T>C were in Hardy-Weinberg disequilibrium (c2C was associated with a greater eye muscle area and the TT genotype at g.13232C>T was associated with greater intramuscular fat. When these genotypes were combined there was no difference in eye muscle area and intramuscular fat between the diplotypes. The H H diplotype was associated with carcass traits that are likely to provide economic advantage in Qinchuan cattle. Variations in the FASN genes and their corresponding genotypes may be considered as molecular markers for economic traits in cattle breeding.
[Mh] Termos MeSH primário: Ácido Graxo Sintase Tipo I/genética
Estudos de Associação Genética/métodos
Polimorfismo de Nucleotídeo Único
[Mh] Termos MeSH secundário: Tecido Adiposo Branco/metabolismo
Animais
Composição Corporal
Bovinos
Feminino
Carne
Locos de Características Quantitativas
Seleção Artificial
Análise de Sequência de DNA
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 2.3.1.85 (Fatty Acid Synthase, Type I)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180129
[Lr] Data última revisão:
180129
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171224
[St] Status:MEDLINE


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[PMID]:29061815
[Au] Autor:Sokolowska E; Presler M; Goyke E; Milczarek R; Swierczynski J; Sledzinski T
[Ad] Endereço:Department of Pharmaceutical Biochemistry, Medical University of Gdansk, Gdansk, Poland.
[Ti] Título:Orlistat Reduces Proliferation and Enhances Apoptosis in Human Pancreatic Cancer Cells (PANC-1).
[So] Source:Anticancer Res;37(11):6321-6327, 2017 11.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIM: Pancreatic cancer is a disease with very poor prognosis, and none of currently available pharmacotherapies have proven to be efficient in this indication. The aim of this study was to analyze the expression of fatty acid synthase (FASN) gene as a potential therapeutic target in proliferating human pancreatic cancer cells (PANC-1), and verify if orlistat, originally developed as an anti-obesity drug, inhibits PANC-1 proliferation. MATERIALS AND METHODS: The effects of orlistat on gene expression, lipogenesis, proliferation and apoptosis was studied in PANC-1 cell culture. RESULTS: Expression of FASN increased during proliferation of PANC-1. Inhibition of FASN by orlistat resulted in a significant reduction of PANC-1 proliferation and enhanced apoptosis of these cells. CONCLUSION: This study showed, to our knowledge for the first time, that orlistat exhibits significant antitumor activity against PANC-1 cells. This implies that orlistat analogs with good oral bioavailability may find application in pharmacotherapy of pancreatic cancer.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Ácido Graxo Sintase Tipo I/genética
Lactonas/farmacologia
Neoplasias Pancreáticas/metabolismo
[Mh] Termos MeSH secundário: Apoptose
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Ácido Graxo Sintase Tipo I/metabolismo
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Lipogênese/efeitos dos fármacos
Neoplasias Pancreáticas/tratamento farmacológico
Neoplasias Pancreáticas/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Lactones); 95M8R751W8 (orlistat); EC 2.3.1.85 (FASN protein, human); EC 2.3.1.85 (Fatty Acid Synthase, Type I)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171026
[Lr] Data última revisão:
171026
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171025
[St] Status:MEDLINE


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[PMID]:28848043
[Au] Autor:Young KE; Flaherty S; Woodman KM; Sharma-Walia N; Reynolds JM
[Ad] Endereço:Department of Microbiology and Immunology, Chicago Medical School, Rosalind Franklin University of Medicine and Science, North Chicago, Illinois, USA.
[Ti] Título:Fatty acid synthase regulates the pathogenicity of Th17 cells.
[So] Source:J Leukoc Biol;102(5):1229-1235, 2017 Nov.
[Is] ISSN:1938-3673
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:T cell activation and effector function is characterized by changes in metabolism. Altered metabolism is common to almost all types of activated T cells, but fatty acid synthesis seems to especially drive the formation of Th17 cells. Indeed, research has demonstrated that inhibition of early fatty acid synthesis through targeting of acetyl-CoA carboxylase (ACC1) can inhibit Th17 cell formation and instead promote the generation of regulatory T cells. Fatty acid synthase (FASN) is downstream of ACC, and previous studies have shown that FASN activity influences both cancer and inflammation. However, it remains to be determined whether FASN is a viable target for inhibiting Th17 cell function. Here, we demonstrate that FASN is a critical metabolic control for the generation of inflammatory subsets of Th17 cells. Conversely, inhibiting FASN function promotes IFN-γ production by Th1 and Th1-like Th17 cells. In vivo, inhibition of FASN, specifically in Th17 cells, leads to reduction of experimental autoimmune encephalomyelitis disease. These studies demonstrate the necessity of FASN in the autoimmune inflammatory function of Th17 cells.
[Mh] Termos MeSH primário: Encefalomielite Autoimune Experimental/imunologia
Ácido Graxo Sintase Tipo I/imunologia
Interferon gama/imunologia
Interleucina-17/imunologia
Células Th17/imunologia
[Mh] Termos MeSH secundário: 4-Butirolactona/análogos & derivados
4-Butirolactona/farmacologia
Animais
Diferenciação Celular
Encefalomielite Autoimune Experimental/induzido quimicamente
Encefalomielite Autoimune Experimental/tratamento farmacológico
Encefalomielite Autoimune Experimental/genética
Inibidores Enzimáticos/farmacologia
Ácido Graxo Sintase Tipo I/antagonistas & inibidores
Ácido Graxo Sintase Tipo I/genética
Regulação da Expressão Gênica
Seres Humanos
Interferon gama/genética
Interleucina-17/genética
Interleucina-23/genética
Interleucina-23/imunologia
Ativação Linfocitária
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Glicoproteína Mielina-Oligodendrócito
Fragmentos de Peptídeos
Cultura Primária de Células
Transdução de Sinais
Linfócitos T Reguladores/efeitos dos fármacos
Linfócitos T Reguladores/imunologia
Linfócitos T Reguladores/patologia
Células Th1/efeitos dos fármacos
Células Th1/imunologia
Células Th1/patologia
Células Th17/efeitos dos fármacos
Células Th17/patologia
Receptor 2 Toll-Like/genética
Receptor 2 Toll-Like/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (4-methylene-2-octyl-5-oxofuran-3-carboxylic acid); 0 (Enzyme Inhibitors); 0 (Interleukin-17); 0 (Interleukin-23); 0 (Myelin-Oligodendrocyte Glycoprotein); 0 (Peptide Fragments); 0 (Tlr2 protein, mouse); 0 (Toll-Like Receptor 2); 0 (myelin oligodendrocyte glycoprotein (35-55)); 82115-62-6 (Interferon-gamma); EC 2.3.1.85 (Fatty Acid Synthase, Type I); OL659KIY4X (4-Butyrolactone)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171109
[Lr] Data última revisão:
171109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170830
[St] Status:MEDLINE
[do] DOI:10.1189/jlb.3AB0417-159RR


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[PMID]:28810876
[Au] Autor:Nowacka-Woszuk J; Madeja ZE; Chmurzynska A
[Ad] Endereço:Department of Genetics and Animal Breeding, Poznan University of Life Sciences, Wolynska 33, 60-637, Poznan, Poland.
[Ti] Título:Prenatal caloric restriction alters lipid metabolism but not hepatic Fasn gene expression and methylation profiles in rats.
[So] Source:BMC Genet;18(1):78, 2017 Aug 15.
[Is] ISSN:1471-2156
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Undernutrition is an increasingly common problem. Insufficient calorie intake and nutrient deficiencies during pregnancy may have an impact not only on the mother, but may also alter metabolism in the infant. In this study, we have applied a calorie-restricted diet during gestation and examined its effect on hepatic Fasn mRNA and DNA methylation profiles in rats and their female progeny. The body composition and blood lipid profiles were also evaluated in both generations. RESULTS: The results showed that the investigated diet regimen exerted a greater effect on the dams than on the offspring. We found that, in the calorie-restricted group, the transcript level of the Fasn gene in the liver increased in the mothers, while in the progeny it was only slightly enhanced. The implemented diet altered lipid profile in the dams by decreasing total cholesterol, HDL, and TG levels. An increase in LDL was noted in the offspring. No change in DNA methylation profile was observed in response to the calorie-restricted diet. CONCLUSIONS: Calorie restriction during pregnancy modified the hepatic Fasn mRNA transcript level and altered the blood cholesterol concentrations in dams, but there were no such effects in their four-week-old offspring. The examined dietary regimen had no effect on DNA methylation of the Fasn 5'-flanking region in the rat liver.
[Mh] Termos MeSH primário: Restrição Calórica
Metilação de DNA
Ácido Graxo Sintase Tipo I/metabolismo
Regulação da Expressão Gênica
Metabolismo dos Lipídeos
Fígado/metabolismo
[Mh] Termos MeSH secundário: Regiões 5' não Traduzidas
Animais
Glicemia/metabolismo
Colesterol/sangue
Ácido Graxo Sintase Tipo I/genética
Feminino
Masculino
Gravidez
RNA Mensageiro/genética
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (5' Untranslated Regions); 0 (Blood Glucose); 0 (RNA, Messenger); 97C5T2UQ7J (Cholesterol); EC 2.3.1.85 (FASN protein, rat); EC 2.3.1.85 (Fatty Acid Synthase, Type I)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171103
[Lr] Data última revisão:
171103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170817
[St] Status:MEDLINE
[do] DOI:10.1186/s12863-017-0544-0


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[PMID]:28729415
[Au] Autor:Stepanova DS; Semenova G; Kuo YM; Andrews AJ; Ammoun S; Hanemann CO; Chernoff J
[Ad] Endereço:Pirogov Russian National Research Medical University, Moscow, Russia.
[Ti] Título:An Essential Role for the Tumor-Suppressor Merlin in Regulating Fatty Acid Synthesis.
[So] Source:Cancer Res;77(18):5026-5038, 2017 Sep 15.
[Is] ISSN:1538-7445
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Neurofibromatosis type 2 (NF2) is an autosomal dominant disorder characterized by the development of multiple tumors in the central nervous system, most notably schwannomas, and meningiomas. Mutational inactivation of the gene encoding the protein Merlin is found in most sporadic and inherited schwannomas, but the molecular mechanisms underlying neoplastic changes in schwannoma cells remain unclear. We report here that Nf2-deficient cells display elevated expression levels of key enzymes involved in lipogenesis and that this upregulation is caused by increased activity of Torc1. Inhibition or knockdown of fatty acid synthase (FASN), the enzyme that catalyzes the formation of palmitic acid from malonyl-CoA, drove -deficient cells into apoptosis. Treatment of -mutant cells with agents that inhibit the production of malonyl-CoA reduced their sensitivity to FASN inhibitors. Collectively, these results suggest that the altered lipid metabolism found in -mutant cells renders them sensitive to elevated levels of malonyl-CoA, as occurs following blockade of FASN, suggesting new targeted strategies in the treatment of -deficient tumors. .
[Mh] Termos MeSH primário: Biomarcadores Tumorais/metabolismo
Ácido Graxo Sintase Tipo I/metabolismo
Ácidos Graxos/metabolismo
Meningioma/patologia
Complexos Multiproteicos/metabolismo
Neurilemoma/patologia
Neurofibromina 2/metabolismo
Serina-Treonina Quinases TOR/metabolismo
[Mh] Termos MeSH secundário: Animais
Apoptose
Biomarcadores Tumorais/genética
Proliferação Celular
Células Cultivadas
Embrião de Mamíferos/citologia
Embrião de Mamíferos/metabolismo
Ácido Graxo Sintase Tipo I/genética
Feminino
Fibroblastos/citologia
Fibroblastos/metabolismo
Seres Humanos
Lipogênese
Alvo Mecanístico do Complexo 1 de Rapamicina
Neoplasias Meníngeas/genética
Neoplasias Meníngeas/metabolismo
Neoplasias Meníngeas/patologia
Meningioma/genética
Meningioma/metabolismo
Camundongos
Camundongos Nus
Complexos Multiproteicos/genética
Neurilemoma/genética
Neurilemoma/metabolismo
Neurofibromina 2/genética
Ratos
Taxa de Sobrevida
Serina-Treonina Quinases TOR/genética
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (Fatty Acids); 0 (Multiprotein Complexes); 0 (Neurofibromin 2); EC 2.3.1.85 (FASN protein, human); EC 2.3.1.85 (Fatty Acid Synthase, Type I); EC 2.7.1.1 (TOR Serine-Threonine Kinases); EC 2.7.11.1 (Mechanistic Target of Rapamycin Complex 1)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170722
[St] Status:MEDLINE
[do] DOI:10.1158/0008-5472.CAN-16-2834


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[PMID]:28668964
[Au] Autor:Chen J; Zhao H; Ma X; Zhang Y; Lu S; Wang Y; Zong C; Qin D; Wang Y; Yingfeng Yang Y; Wang X; Liu Y
[Ad] Endereço:Department of Cell Biology, Shandong University School of Medicine, Jinan, China.
[Ti] Título:GLP-1/GLP-1R Signaling in Regulation of Adipocyte Differentiation and Lipogenesis.
[So] Source:Cell Physiol Biochem;42(3):1165-1176, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: The aim of this study was to determine the direct role of liraglutide (LG) in adipogenesis and lipid metabolism. METHODS: Lipid accumulation was evaluated by oil red O staining, quantitative real-time PCR (qPCR) was performed to determine glucagon-like peptide 1 receptor (GLP-1R), fatty acid synthase (FASN) and adipose triglyceride lipase (ATGL) expression in 3T3-L1 preadipocytes, differentiated adipocytes and in adipose tissues from mice. The effects of LG on 3T3-L1 adipogenesis and lipid metabolism were analyzed with qPCR, Western Blotting, oil red O staining, immunohistochemistry (IHC) and immunofluorescence (IF). All measurements were performed at least three times. RESULTS: LG increased the expression of differentiation marker genes and lipid accumulation during preadipocyte differentiation. In differentiated adipocytes, LG decreased FASN expression, and simultaneously led to CREB phosphorylation and ERK1/2 activation which were abolished by a GLP-1R antagonist, exendin (9-39). LG induced-FASN down-regulation was partially reversed by PKA and ERK1/2 inhibitors. Consistent with above in vitro findings, LG treatment significantly reduced FASN expression in visceral adipose tissues of ob/ob mice, and reduced body weight gain. CONCLUSION: LG promotes preadipocytes differentiation, and inhibits FASN expression in adipocytes. LG induced down-regulation of FASN is at least partially mediated by PKA and MAPK signaling pathways.
[Mh] Termos MeSH primário: Adipócitos/efeitos dos fármacos
Adipogenia/efeitos dos fármacos
Peptídeo 1 Semelhante ao Glucagon/metabolismo
Receptor do Peptídeo Semelhante ao Glucagon 1/metabolismo
Hipoglicemiantes/farmacologia
Lipogênese/efeitos dos fármacos
Liraglutida/farmacologia
[Mh] Termos MeSH secundário: Células 3T3-L1
Adipócitos/citologia
Adipócitos/metabolismo
Animais
Regulação para Baixo/efeitos dos fármacos
Ácido Graxo Sintase Tipo I/genética
Ácido Graxo Sintase Tipo I/metabolismo
Peptídeo 1 Semelhante ao Glucagon/genética
Receptor do Peptídeo Semelhante ao Glucagon 1/genética
Camundongos
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glucagon-Like Peptide-1 Receptor); 0 (Hypoglycemic Agents); 839I73S42A (Liraglutide); 89750-14-1 (Glucagon-Like Peptide 1); EC 2.3.1.85 (Fatty Acid Synthase, Type I)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170703
[St] Status:MEDLINE
[do] DOI:10.1159/000478872


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[PMID]:28639885
[Au] Autor:Xu Z; Li C; Qu H; Li H; Gu Q; Xu J
[Ad] Endereço:1 Department of Emergency, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, P.R. China.
[Ti] Título:MicroRNA-195 inhibits the proliferation and invasion of pancreatic cancer cells by targeting the fatty acid synthase/Wnt signaling pathway.
[So] Source:Tumour Biol;39(6):1010428317711324, 2017 Jun.
[Is] ISSN:1423-0380
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Emerging evidence suggests that microRNAs are critical regulators of cancer development and progression. MicroRNA-195 has been reported as a cancer-related microRNA in many human cancers. However, the role of microRNA-195 in pancreatic cancer remains largely unknown. Here, we show that microRNA-195 is downregulated in pancreatic cancer tissues and cell line. Also, we show that overexpression of microRNA-195 inhibits the proliferation and invasion of pancreatic cancer cells, whereas suppression of microRNA-195 promotes proliferation and invasion. We show that microRNA-195 directly targets the fatty acid synthase enzyme and negatively regulates the expression of fatty acid synthase. Also, we show that fatty acid synthase expression is inversely correlated with microRNA-195 expression in pancreatic cancer tissues. Moreover, our results show that microRNA-195 inhibits Wnt signaling in pancreatic cancer cells. By restoring fatty acid synthase expression, we were able to reverse the antitumor effects of microRNA-195 in pancreatic cancer cells. Taken together, our findings show that microRNA-195 inhibits pancreatic cancer cell proliferation and invasion by regulating the fatty acid synthase/Wnt signaling pathway, suggesting a tumor suppressive role for microRNA-195 in the development and progression of pancreatic cancer. Thus, inhibiting fatty acid synthase by microRNA-195 may serve as a novel therapeutic approach for the treatment of pancreatic cancer.
[Mh] Termos MeSH primário: Proliferação Celular/genética
Ácido Graxo Sintase Tipo I/genética
MicroRNAs/genética
Neoplasias Pancreáticas/genética
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Movimento Celular
Ácido Graxo Sintase Tipo I/biossíntese
Feminino
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Masculino
Invasividade Neoplásica/genética
Invasividade Neoplásica/patologia
Neoplasias Pancreáticas/patologia
Via de Sinalização Wnt/genética
beta Catenina/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MIRN195 microRNA, human); 0 (MicroRNAs); 0 (beta Catenin); EC 2.3.1.85 (FASN protein, human); EC 2.3.1.85 (Fatty Acid Synthase, Type I)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170713
[Lr] Data última revisão:
170713
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170623
[St] Status:MEDLINE
[do] DOI:10.1177/1010428317711324


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[PMID]:28623919
[Au] Autor:Saad DY; Soliman MM; Baiomy AA; Yassin MH; El-Sawy HB
[Ad] Endereço:Medical Laboratory Department, Faculty of Applied Medical Sciences, Taif University, Turabah, Saudi Arabia.
[Ti] Título:Effects of Karela (Bitter Melon; Momordica charantia) on genes of lipids and carbohydrates metabolism in experimental hypercholesterolemia: biochemical, molecular and histopathological study.
[So] Source:BMC Complement Altern Med;17(1):319, 2017 Jun 17.
[Is] ISSN:1472-6882
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Hypercholesterolemia is a serious diseases associated with type-2 diabetes, atherosclerosis, cardiovascular disorders and liver diseases. Humans seek for safe herbal medication such as karela (Momordica charantia/bitter melon) to treat such disorders to avoid side effect of pharmacotherapies widely used. METHODS: Forty male Wistar rats were divided into four equal groups; control group with free access to food and water, cholesterol administered group (40 mg/kg BW orally); karela administered group (5 g /kg BW orally) and mixture of cholesterol and karela. The treatments continued for 10 weeks. Karela was given for hypercholesterolemic rats after 6 weeks of cholesterol administration. Serum, liver and epididymal adipose tissues were taken for biochemical, histopathological and genetic assessments. RESULTS: Hypercholesterolemia induced a decrease in serum superoxide dismutase (SOD), catalase, reduced glutathione (GSH) and an increase in malondialdehyde (MDA) levels that were ameliorated by karela administration. Hypercholesterolemia up regulated antioxidants mRNA expression and altered the expression of carbohydrate metabolism genes. In parallel, hypercholesterolemic groups showed significant changes in the expression of PPAR-alpha and gamma, lipolysis, lipogenesis and cholesterol metabolism such as carnitine palmitoyltransferase-1 (CPT-1). Acyl CoA oxidase (ACO), fatty acids synthase (FAS), sterol responsible element binding protein-1c (SREBP1c), 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMG-CoAR) and cholesterol 7α-hydroxylase (CYP7A1) at hepatic and adipose tissue levels. Interestingly, Karela ameliorated all altered genes confirming its hypocholesterolemic effect. Histopathological and immunohistochemical findings revealed that hypercholesterolemia induced hepatic tissue changes compared with control. These changes include cholesterol clefts, necrosis, karyolysis and sever congestion of portal blood vessel. Caspase-3 immunoreactivity showed positive expression in hepatic cells of hypercholesterolemic rats compared to control. All were counteracted and normalized after Karela administration to hypercholesterolemic group. CONCLUSION: Current findings confirmed that karela is a potential supplement useful in treatment of hypercholesterolemia and its associated disorders and is good for human health.
[Mh] Termos MeSH primário: Metabolismo dos Carboidratos
Hipercolesterolemia/dietoterapia
Hipercolesterolemia/genética
Metabolismo dos Lipídeos
Momordica charantia/metabolismo
[Mh] Termos MeSH secundário: Tecido Adiposo/metabolismo
Animais
Anticolesterolemiantes/metabolismo
Colesterol/metabolismo
Colesterol 7-alfa-Hidroxilase/genética
Colesterol 7-alfa-Hidroxilase/metabolismo
Ácido Graxo Sintase Tipo I/genética
Ácido Graxo Sintase Tipo I/metabolismo
Seres Humanos
Hipercolesterolemia/enzimologia
Hipercolesterolemia/metabolismo
Fígado/metabolismo
Masculino
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anticholesteremic Agents); 97C5T2UQ7J (Cholesterol); EC 1.14.14.23 (Cholesterol 7-alpha-Hydroxylase); EC 2.3.1.85 (Fatty Acid Synthase, Type I)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170821
[Lr] Data última revisão:
170821
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170619
[St] Status:MEDLINE
[do] DOI:10.1186/s12906-017-1833-x


  9 / 341 MEDLINE  
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[PMID]:28570839
[Au] Autor:Li G; Ning C; Ma Y; Jin L; Tang Q; Li X; Li M; Liu H
[Ad] Endereço:Farm Animal Genetic Resources Exploration and Innovation Key Laboratory of Sichuan Province, Sichuan Agricultural University , Chengdu, People's Republic of China .
[Ti] Título:miR-26b Promotes 3T3-L1 Adipocyte Differentiation Through Targeting PTEN.
[So] Source:DNA Cell Biol;36(8):672-681, 2017 Aug.
[Is] ISSN:1557-7430
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:microRNAs (miRNAs) play important roles in adipogenesis that is closely linked to obesity and energy homeostasis. Thus far, only a few miRNAs have been identified to regulate adipocyte development, arousing interest in the detailed function of miRNAs during adipogenesis. In this study, we found that the miR-26b expression showed an increasing trend during 3T3-L1 cells differentiation. To investigate the role of miR-26b in adipogenesis, the synthetic miR-26b agomirs and antagomirs were used to perform overexpression and knockdown experiment, respectively. Our data revealed that overexpression of miR-26b significantly accelerated the mRNA expression of the adipogenic markers, peroxisome proliferator-activated receptor gamma (PPARγ), fatty acid synthase (FAS), CCAAT/enhancer binding protein alpha (C/EBPα), and lipoprotein lipase, and the protein level of PPARγ and FAS. miR-26b overexpression also resulted in a significant increase in lipid accumulation. In contrast, inhibition of miR-26b expression decreased differentiation of 3T3-L1 cells. By target gene prediction and luciferase reporter assay, we demonstrated that miR-26b may directly bind to the 3' UTR of phosphatase and tensin homolog (PTEN). Taken together, these results demonstrate that miR-26b might participate in regulating adipogenic differentiation in 3T3-L1 cells by inhibiting the PTEN expression, further highlighting the importance of miRNA in adipogenesis.
[Mh] Termos MeSH primário: Adipócitos/fisiologia
Adipogenia/genética
MicroRNAs/fisiologia
PTEN Fosfo-Hidrolase/genética
[Mh] Termos MeSH secundário: Células 3T3-L1
Adipócitos/citologia
Animais
Proteína alfa Estimuladora de Ligação a CCAAT/biossíntese
Proteína alfa Estimuladora de Ligação a CCAAT/genética
Ácido Graxo Sintase Tipo I/biossíntese
Ácido Graxo Sintase Tipo I/genética
Expressão Gênica
Células HeLa
Seres Humanos
Metabolismo dos Lipídeos/genética
Metabolismo dos Lipídeos/fisiologia
Camundongos
MicroRNAs/genética
PPAR gama/biossíntese
PPAR gama/genética
Reação em Cadeia da Polimerase em Tempo Real
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCAAT-Enhancer-Binding Protein-alpha); 0 (MicroRNAs); 0 (Mirn26 microRNA, mouse); 0 (PPAR gamma); EC 2.3.1.85 (Fatty Acid Synthase, Type I); EC 3.1.3.67 (PTEN Phosphohydrolase); EC 3.1.3.67 (Pten protein, mouse)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170602
[St] Status:MEDLINE
[do] DOI:10.1089/dna.2017.3712


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[PMID]:28549068
[Au] Autor:Camargo N; Goudriaan A; van Deijk AF; Otte WM; Brouwers JF; Lodder H; Gutmann DH; Nave KA; Dijkhuizen RM; Mansvelder HD; Chrast R; Smit AB; Verheijen MHG
[Ad] Endereço:Department of Molecular and Cellular Neurobiology, Center for Neurogenomics and Cognitive Research, Amsterdam Neuroscience, VU University Amsterdam, Amsterdam, the Netherlands.
[Ti] Título:Oligodendroglial myelination requires astrocyte-derived lipids.
[So] Source:PLoS Biol;15(5):e1002605, 2017 May.
[Is] ISSN:1545-7885
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In the vertebrate nervous system, myelination of axons for rapid impulse propagation requires the synthesis of large amounts of lipids and proteins by oligodendrocytes and Schwann cells. Myelin membranes are thought to be cell-autonomously assembled by these axon-associated glial cells. Here, we report the surprising finding that in normal brain development, a substantial fraction of the lipids incorporated into central nervous system (CNS) myelin are contributed by astrocytes. The oligodendrocyte-specific inactivation of sterol regulatory element-binding protein (SREBP) cleavage-activating protein (SCAP), an essential coactivator of the transcription factor SREBP and thus of lipid biosynthesis, resulted in significantly retarded CNS myelination; however, myelin appeared normal at 3 months of age. Importantly, embryonic deletion of the same gene in astrocytes, or in astrocytes and oligodendrocytes, caused a persistent hypomyelination, as did deletion from astrocytes during postnatal development. Moreover, when astroglial lipid synthesis was inhibited, oligodendrocytes began incorporating circulating lipids into myelin membranes. Indeed, a lipid-enriched diet was sufficient to rescue hypomyelination in these conditional mouse mutants. We conclude that lipid synthesis by oligodendrocytes is heavily supplemented by astrocytes in vivo and that horizontal lipid flux is a major feature of normal brain development and myelination.
[Mh] Termos MeSH primário: Astrócitos/metabolismo
Doenças Desmielinizantes/metabolismo
Peptídeos e Proteínas de Sinalização Intracelular/metabolismo
Metabolismo dos Lipídeos
Proteínas de Membrana/metabolismo
Bainha de Mielina/metabolismo
Oligodendroglia/metabolismo
Proteína de Ligação a Elemento Regulador de Esterol 2/metabolismo
[Mh] Termos MeSH secundário: Animais
Astrócitos/patologia
Astrócitos/ultraestrutura
Biomarcadores/metabolismo
Cruzamentos Genéticos
Doenças Desmielinizantes/patologia
Doenças Desmielinizantes/prevenção & controle
Dieta Hiperlipídica
Ácido Graxo Sintase Tipo I/metabolismo
Deleção de Genes
Proteína Glial Fibrilar Ácida/genética
Proteína Glial Fibrilar Ácida/metabolismo
Seres Humanos
Peptídeos e Proteínas de Sinalização Intracelular/genética
Proteínas de Membrana/genética
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Microscopia Eletrônica de Transmissão
Mutação
Bainha de Mielina/patologia
Bainha de Mielina/ultraestrutura
Proteínas do Tecido Nervoso/genética
Proteínas do Tecido Nervoso/metabolismo
Oligodendroglia/patologia
Oligodendroglia/ultraestrutura
Especificidade de Órgãos
Processamento de Proteína Pós-Traducional
Proteína de Ligação a Elemento Regulador de Esterol 2/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Glial Fibrillary Acidic Protein); 0 (Intracellular Signaling Peptides and Proteins); 0 (Membrane Proteins); 0 (Nerve Tissue Proteins); 0 (SREBP cleavage-activating protein); 0 (Srebf2 protein, mouse); 0 (Sterol Regulatory Element Binding Protein 2); EC 2.3.1.85 (Fatty Acid Synthase, Type I)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170527
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pbio.1002605



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