Base de dados : MEDLINE
Pesquisa : G02.111.528 [Categoria DeCS]
Referências encontradas : 2038 [refinar]
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  1 / 2038 MEDLINE  
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[PMID]:29272757
[Au] Autor:Liu Z; Kuang W; Xu X; Li D; Zhu W; Lan Z; Zhang X
[Ad] Endereço:School of Medicine, Yangtze University, Jingzhou 434000, China.
[Ti] Título:Putative identification of components in Zengye Decoction and their effects on glucose consumption and lipogenesis in insulin-induced insulin-resistant HepG2 cells.
[So] Source:J Chromatogr B Analyt Technol Biomed Life Sci;1073:145-153, 2018 Jan 15.
[Is] ISSN:1873-376X
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Zengye Decoction (ZYD) is a well-known traditional medicine in China used for treating diseases associated with "Yin deficiency" such as diabetes. However, little information is available on its components, pharmacological effects and underlying mechanisms. This study was designed to identify its active components and evaluate the effects and mechanisms of ZYD on glucose consumption and lipogenesis in insulin-induced insulin-resistant (IR)-HepG2 cells. In this study, 45 compounds of ZYD were putatively identified, in which the iridoid glycosides such as catalpol, aucubin and harpagide were identified as the main components. The insulin-resistant (IR)-HepG2 cell model was established and the effect of ZYD at three doses (0.17, 0.5 and 1.5 µg/mL) on cell growth was evaluated with an IncuCyte™ live-cell imaging system. The effects of ZYD on glucose consumption and uptake were evaluated by glucose consumption and uptake assay. Meanwhile, the effect of ZYD on lipogenesis was investigated in IR-HepG2 cells by oil red O (ORO) staining. Western blot was applied to observe the changes in some of the key factors involved in glucose metabolism and lipogenesis. It was found that the ZYD at a dose of 1.5 µg/mL exhibited an inhibitory activity on IR-HepG2 cell growth. Besides, ZYD at doses of 0.5 and 1.5 µg/mL accelerated the glucose consumption, glucose uptake and reduced the lipogenesis in the IR-HepG2 cells. Western blot studies revealed that ZYD phosphorylated AMP-activated protein kinase α subunits (AMPKα), upregulated hexokinase (HK), phosphorylated acetyl-CoA carboxylase alpha (pACC1) and carnitine palmitoyltransferase 1A (CPT1A) in the IR-HepG2 cells. These results indicate ZYD promotes glucose consumption and uptake, and attenuates lipogenesis in IR-HepG2 cells, which may be involved in activating AMPK and regulating its downstream factors including HK, pACC1 and CPT1A.
[Mh] Termos MeSH primário: Medicamentos de Ervas Chinesas/farmacologia
Glucose/metabolismo
Resistência à Insulina
Insulina/metabolismo
Lipogênese/efeitos dos fármacos
[Mh] Termos MeSH secundário: Proteínas Quinases Ativadas por AMP/metabolismo
Glicólise/efeitos dos fármacos
Células Hep G2
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Drugs, Chinese Herbal); 0 (Insulin); EC 2.7.11.31 (AMP-Activated Protein Kinases); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171223
[St] Status:MEDLINE


  2 / 2038 MEDLINE  
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[PMID]:29323924
[Au] Autor:Zhang T; Huang J; Yi Y; Zhang X; Loor JJ; Cao Y; Shi H; Luo J
[Ad] Endereço:Shanxi Key Laboratory of Molecular Biology for Agriculture, College of Animal Science and Technology, Northwest A&F University , Yangling, Shaanxi 712100, PR China.
[Ti] Título:Akt Serine/Threonine Kinase 1 Regulates de Novo Fatty Acid Synthesis through the Mammalian Target of Rapamycin/Sterol Regulatory Element Binding Protein 1 Axis in Dairy Goat Mammary Epithelial Cells.
[So] Source:J Agric Food Chem;66(5):1197-1205, 2018 Feb 07.
[Is] ISSN:1520-5118
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Akt serine/threonine kinase acts as a central mediator in the phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway, regulating a series of biological processes. In lipid metabolism, Akt activation regulates a series of gene expressions, including genes related to intracellular fatty acid synthesis. However, the regulatory mechanisms of Akt in dairy goat mammary lipid metabolism have not been elaborated. In this study, the coding sequences of goat Akt1 gene were cloned and analyzed. Gene expression of Akt1 in different lactation stages was also investigated. For in vitro studies, a eukaryotic expression vector of Akt1 was constructed and transfected to goat mammary epithelial cells (GMECs), and specific inhibitors of Akt/mammalian target of rapamycin (mTOR) signaling were applied to GMECs. Results showed that Akt1 protein was highly conserved, and its mRNA was highly expressed in midlactation. In vitro studies indicated that Akt1 phosphorylation activated mTOR and subsequently enhanced sterol regulatory element binding protein 1 (SREBP1), thus increasing intracellular triacylglycerol content. Inhibition of Akt/mTOR signaling down-regulated the gene expression of lipogenic genes. Overall, Akt1 plays an important role in regulating de novo fatty acid synthesis in goat mammary epithelial cells, and this process probably is through the mTOR/SREBP1 axis.
[Mh] Termos MeSH primário: Ácidos Graxos/biossíntese
Cabras
Glândulas Mamárias Animais/metabolismo
Proteínas Proto-Oncogênicas c-akt/fisiologia
Proteína de Ligação a Elemento Regulador de Esterol 1/fisiologia
Serina-Treonina Quinases TOR/fisiologia
[Mh] Termos MeSH secundário: Animais
Epitélio/metabolismo
Regulação da Expressão Gênica/fisiologia
Lipogênese/genética
Proteínas Proto-Oncogênicas c-akt/genética
Transdução de Sinais/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fatty Acids); 0 (Sterol Regulatory Element Binding Protein 1); EC 2.7.1.1 (TOR Serine-Threonine Kinases); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180112
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jafc.7b05305


  3 / 2038 MEDLINE  
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[PMID]:29198881
[Au] Autor:Renu K; Madhyastha H; Madhyastha R; Maruyama M; Arunachlam S; V G A
[Ad] Endereço:Department of Biomedical Sciences, School of Biosciences and Technology, VIT University, Vellore, Tamil Nadu- 632014, India.
[Ti] Título:Role of arsenic exposure in adipose tissue dysfunction and its possible implication in diabetes pathophysiology.
[So] Source:Toxicol Lett;284:86-95, 2018 Mar 01.
[Is] ISSN:1879-3169
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Exposure to arsenic in drinking water can stimulate a diverse number of diseases that originate from impaired lipid metabolism in adipose and glucose metabolism, leading to insulin resistance. Arsenic inhibits differentiation of adipocyte and mediates insulin resistance with diminutive information on arsenicosis on lipid storage and lipolysis. This review focused on different mechanisms and pathways involved in adipogenesis and lipolysis in adipose tissue during arsenic-induced diabetes. Though arsenic is known to cause type2 diabetes through different mechanisms, the role of adipose tissue in causing type2 diabetes is still unclear. With the existing literature, this review exhibits the effect of arsenic on adipose tissue and its signalling events such as SIRT3- FOXO3a signalling pathway, Ras -MAP -AP-1 cascade, PI(3)-K-Akt pathway, endoplasmic reticulum stress protein, C/EBP homologous protein (CHOP10) and GPCR pathway with role of adipokines. There is a need to elucidate the different types of adipokines which are involved in arsenic-induced diabetes. The exhibited information brings to light that arsenic has negative effects on a white adipose tissue (WAT) by decreasing adipogenesis and enhancing lipolysis. Some of the epidemiological studies show that arsenic would causes obesity. Few studies indicate that arsenic might induces lipodystrophy condition. Further research is needed to evaluate the mechanistic link between arsenic and adipose tissue dysfunction which leads to insulin resistance.
[Mh] Termos MeSH primário: Adipogenia/efeitos dos fármacos
Tecido Adiposo Branco/efeitos dos fármacos
Arsênico/toxicidade
Diabetes Mellitus Tipo 2/induzido quimicamente
Poluentes Ambientais/toxicidade
Lipogênese/efeitos dos fármacos
[Mh] Termos MeSH secundário: Tecido Adiposo Branco/metabolismo
Tecido Adiposo Branco/fisiopatologia
Diabetes Mellitus Tipo 2/metabolismo
Glucose/metabolismo
Seres Humanos
Resistência à Insulina
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Environmental Pollutants); IY9XDZ35W2 (Glucose); N712M78A8G (Arsenic)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171205
[St] Status:MEDLINE


  4 / 2038 MEDLINE  
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[PMID]:28458350
[Au] Autor:Li H; Ying H; Hu A; Hu Y; Li D
[Ad] Endereço:Department of Liver Disease, Ningbo No. 2 Hospital.
[Ti] Título:Therapeutic Effect of Gypenosides on Nonalcoholic Steatohepatitis via Regulating Hepatic Lipogenesis and Fatty Acid Oxidation.
[So] Source:Biol Pharm Bull;40(5):650-657, 2017.
[Is] ISSN:1347-5215
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Nonalcoholic steatohepatitis (NASH) is the most frequent cause of liver dysfunction and a common global problem. Gypenosides can decrease pathological modifications of high-fat diet-induced rat atherosclerosis; however, its effect and mechanism on NASH remain unclear. In this study, rats were randomly divided into normal control and model groups. Model rats were fed with a high-fat diet and treated with gypenosides, rosiglitazone, or water for 6 weeks. We found that liver tissues showed significant hepatic steatosis and vacuolar degeneration with significantly higher triglyceride (TG), free fatty acid (FFA) and malonyl CoA, serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and gamma-glutamyl transferase (GGT) activities in model group versus normal control group (p<0.01). Liver tissue mRNA and protein levels of sterol regulatory element binding protein-1c (SREBP-1c), carbohydrate response element binding protein (ChREBP), acetyl-CoA carboxylase (ACCase), and stearoyl CoA desaturase enzyme 1 (SCD1) were significantly increased, while the carnitine palmitoyl transferase-1 (CPT-1) level was significantly decreased in the model group versus the normal control group (p<0.01). Pathological changes of hepatic steatosis; body weight and liver wet weight; liver tissue TG, FFA and malonyl CoA concentrations; serum ALT, AST and GGT activities; liver tissue mRNA and protein levels of SREBP-1c, ChREBP, ACCase, and SCD-1 were significantly decreased; protein and mRNA levels of CPT-1 were significantly increased in the gypenosides group versus model group (p<0.01). In conclusion, gypenosides has therapeutic effect on NASH through regulating key transcriptional factors and lipogenic enzymes involved in fatty acid oxidation during hepatic lipogenesis.
[Mh] Termos MeSH primário: Ácidos Graxos/metabolismo
Lipogênese/efeitos dos fármacos
Fígado/metabolismo
Hepatopatia Gordurosa não Alcoólica/tratamento farmacológico
Hepatopatia Gordurosa não Alcoólica/metabolismo
[Mh] Termos MeSH secundário: Animais
Peso Corporal
Dieta Hiperlipídica/efeitos adversos
Gynostemma
Fígado/efeitos dos fármacos
Fígado/patologia
Testes de Função Hepática
Masculino
Hepatopatia Gordurosa não Alcoólica/patologia
Tamanho do Órgão
Oxirredução
Extratos Vegetais/uso terapêutico
Ratos
Ratos Sprague-Dawley
Tiazolidinedionas/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fatty Acids); 0 (Plant Extracts); 0 (Thiazolidinediones); 0 (gypenoside); 05V02F2KDG (rosiglitazone)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE
[do] DOI:10.1248/bpb.b16-00942


  5 / 2038 MEDLINE  
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[PMID]:28461124
[Au] Autor:Mastrofrancesco A; Ottaviani M; Cardinali G; Flori E; Briganti S; Ludovici M; Zouboulis CC; Lora V; Camera E; Picardo M
[Ad] Endereço:Laboratory of Cutaneous Physiopathology and Integrated Center of Metabolomics Research, San Gallicano Dermatologic Institute, IRCCS, Rome, Italy.
[Ti] Título:Pharmacological PPARγ modulation regulates sebogenesis and inflammation in SZ95 human sebocytes.
[So] Source:Biochem Pharmacol;138:96-106, 2017 08 15.
[Is] ISSN:1873-2968
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The nuclear receptor peroxisome proliferator-activated receptor gamma (PPARγ) controls the expression of genes involved in the regulation of lipid and glucose metabolism, cell proliferation/differentiation as well as inflammatory pathways. Pivotal studies in human sebocytes and isolated sebaceous glands have raised the interesting possibility that compounds acting on PPARγ can modulate sebaceous lipids and inflammation and, as such, may be useful in the treatment of acne. To investigate the role of this receptor in the regulation of lipid synthesis, proliferation and inflammation, we used the SZ95 sebaceous gland cell line stimulated with insulin. In sebocytes, insulin signaling activated the phosphatidylinositide 3-kinase-Akt (PI3K/Akt) and mammalian target of rapamycin (mTOR) pathways, which, in turn, induced high protein/lipid synthesis, increased cell growth and proliferation as well as inflammation. As regards lipogenesis, insulin initially stimulated the formation of unsaturated lipids and then the neosynthesis of lipids. The results showed, that the modulation of PPARγ, counteracted the insulin-induced altered lipogenesis, evident through a decrease in gene expression of key enzymes responsible for the synthesis of fatty acids, and through a reduction of lipid species synthesis analyzed by Oil/Nile Red staining and GC-MS. PPARγ modulation also regulated the insulin-induced proliferation, inhibiting the cell cycle progression and p21WAF1/CIP1 (p21) protein reduction. Moreover, the expression of inflammatory cytokines, induced by insulin or lipopolysaccharide (LPS), was down-modulated. In PPARγ-deficient cells or in the presence of GW9662 antagonist, all these observed effects were abolished, indicating that PPARγ activation plays a role in regulating alteration of lipogenesis, cell proliferation and inflammatory signaling. We demonstrated that selective modulation of PPARγ activity is likely to represent a therapeutic strategy for the treatment of acne.
[Mh] Termos MeSH primário: Regulação da Expressão Gênica
Lipogênese
PPAR gama/metabolismo
Glândulas Sebáceas/metabolismo
Sebo/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Acetanilidas/efeitos adversos
Acetanilidas/farmacologia
Anilidas/efeitos adversos
Anilidas/farmacologia
Anti-Inflamatórios não Esteroides/efeitos adversos
Anti-Inflamatórios não Esteroides/farmacologia
Ciclo Celular/efeitos dos fármacos
Linhagem Celular
Proliferação Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Citocinas/agonistas
Citocinas/metabolismo
Fármacos Dermatológicos/efeitos adversos
Fármacos Dermatológicos/farmacologia
Regulação da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Hipoglicemiantes/antagonistas & inibidores
Hipoglicemiantes/farmacologia
Insulina/farmacologia
Antagonistas da Insulina/efeitos adversos
Antagonistas da Insulina/farmacologia
Lipogênese/efeitos dos fármacos
Lipopolissacarídeos/antagonistas & inibidores
Lipopolissacarídeos/toxicidade
PPAR gama/agonistas
PPAR gama/antagonistas & inibidores
PPAR gama/genética
Fenilpropionatos/efeitos adversos
Fenilpropionatos/farmacologia
Interferência de RNA
Glândulas Sebáceas/citologia
Glândulas Sebáceas/efeitos dos fármacos
Glândulas Sebáceas/imunologia
Sebo/efeitos dos fármacos
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (2-chloro-5-nitrobenzanilide); 0 (Acetanilides); 0 (Anilides); 0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Cytokines); 0 (Dermatologic Agents); 0 (GMG-43AC); 0 (Hypoglycemic Agents); 0 (Insulin); 0 (Insulin Antagonists); 0 (Lipopolysaccharides); 0 (PPAR gamma); 0 (Phenylpropionates); 0 (lipopolysaccharide A)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:180201
[Lr] Data última revisão:
180201
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE


  6 / 2038 MEDLINE  
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[PMID]:28470676
[Au] Autor:Stiede K; Miao W; Blanchette HS; Beysen C; Harriman G; Harwood HJ; Kelley H; Kapeller R; Schmalbach T; Westlin WF
[Ad] Endereço:Nimbus Therapeutics, Cambridge, MA.
[Ti] Título:Acetyl-coenzyme A carboxylase inhibition reduces de novo lipogenesis in overweight male subjects: A randomized, double-blind, crossover study.
[So] Source:Hepatology;66(2):324-334, 2017 08.
[Is] ISSN:1527-3350
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:NDI-010976, an allosteric inhibitor of acetyl-coenzyme A carboxylases (ACC) ACC1 and ACC2, reduces hepatic de novo lipogenesis (DNL) and favorably affects steatosis, inflammation, and fibrosis in animal models of fatty liver disease. This study was a randomized, double-blind, placebo-controlled, crossover trial evaluating the pharmacodynamic effects of a single oral dose of NDI-010976 on hepatic DNL in overweight and/or obese but otherwise healthy adult male subjects. Subjects were randomized to receive either NDI-010976 (20, 50, or 200 mg) or matching placebo in period 1, followed by the alternate treatment in period 2; and hepatic lipogenesis was stimulated with oral fructose administration. Fractional DNL was quantified by infusing a stable isotope tracer, [1- C]acetate, and monitoring C incorporation into palmitate of circulating very low-density lipoprotein triglyceride. Single-dose administration of NDI-010976 was well tolerated at doses up to and including 200 mg. Fructose administration over a 10-hour period stimulated hepatic fractional DNL an average of 30.9 ± 6.7% (mean ± standard deviation) above fasting DNL values in placebo-treated subjects. Subjects administered single doses of NDI-010976 at 20, 50, or 200 mg had significant inhibition of DNL compared to placebo (mean inhibition relative to placebo was 70%, 85%, and 104%, respectively). An inverse relationship between fractional DNL and NDI-010976 exposure was observed with >90% inhibition of fractional DNL associated with plasma concentrations of NDI-010976 >4 ng/mL. CONCLUSION: ACC inhibition with a single dose of NDI-010976 is well tolerated and results in a profound dose-dependent inhibition of hepatic DNL in overweight adult male subjects. Therefore, NDI-010976 could contribute considerable value to the treatment algorithm of metabolic disorders characterized by dysregulated fatty acid metabolism, including nonalcoholic steatohepatitis. (Hepatology 2017;66:324-334).
[Mh] Termos MeSH primário: Acetil-CoA Carboxilase/antagonistas & inibidores
Lipogênese/fisiologia
Hepatopatia Gordurosa não Alcoólica/metabolismo
Sobrepeso/tratamento farmacológico
[Mh] Termos MeSH secundário: Acetil-CoA Carboxilase/administração & dosagem
Administração Oral
Adulto
Índice de Massa Corporal
Estudos Cross-Over
Relação Dose-Resposta a Droga
Método Duplo-Cego
Esquema de Medicação
Seguimentos
Seres Humanos
Masculino
Meia-Idade
Segurança do Paciente
Medição de Risco
Resultado do Tratamento
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
EC 6.4.1.2 (Acetyl-CoA Carboxylase)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180122
[Lr] Data última revisão:
180122
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1002/hep.29246


  7 / 2038 MEDLINE  
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[PMID]:29244870
[Au] Autor:Cedó L; Santos D; Roglans N; Julve J; Pallarès V; Rivas-Urbina A; Llorente-Cortes V; Laguna JC; Blanco-Vaca F; Escolà-Gil JC
[Ad] Endereço:Institut d'Investigacions Biomèdiques (IIB) Sant Pau, Barcelona, Spain.
[Ti] Título:Human hepatic lipase overexpression in mice induces hepatic steatosis and obesity through promoting hepatic lipogenesis and white adipose tissue lipolysis and fatty acid uptake.
[So] Source:PLoS One;12(12):e0189834, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Human hepatic lipase (hHL) is mainly localized on the hepatocyte cell surface where it hydrolyzes lipids from remnant lipoproteins and high density lipoproteins and promotes their hepatic selective uptake. Furthermore, hepatic lipase (HL) is closely associated with obesity in multiple studies. Therefore, HL may play a key role on lipid homeostasis in liver and white adipose tissue (WAT). In the present study, we aimed to evaluate the effects of hHL expression on hepatic and white adipose triglyceride metabolism in vivo. Experiments were carried out in hHL transgenic and wild-type mice fed a Western-type diet. Triglyceride metabolism studies included ß-oxidation and de novo lipogenesis in liver and WAT, hepatic triglyceride secretion, and adipose lipoprotein lipase (LPL)-mediated free fatty acid (FFA) lipolysis and influx. The expression of hHL promoted hepatic triglyceride accumulation and de novo lipogenesis without affecting triglyceride secretion, and this was associated with an upregulation of Srebf1 as well as the main genes controlling the synthesis of fatty acids. Transgenic mice also exhibited more adiposity and an increased LPL-mediated FFA influx into the WAT without affecting glucose tolerance. Our results demonstrate that hHL promoted hepatic steatosis in mice mainly by upregulating de novo lipogenesis. HL also upregulated WAT LPL and promoted triglyceride-rich lipoprotein hydrolysis and adipose FFA uptake. These data support the important role of hHL in regulating hepatic lipid homeostasis and confirm the broad cardiometabolic role of HL.
[Mh] Termos MeSH primário: Fígado Gorduroso/genética
Lipase/genética
Obesidade/genética
Proteína de Ligação a Elemento Regulador de Esterol 1/genética
[Mh] Termos MeSH secundário: Tecido Adiposo Branco/metabolismo
Tecido Adiposo Branco/patologia
Animais
Dieta Ocidental
Ácidos Graxos/metabolismo
Fígado Gorduroso/metabolismo
Fígado Gorduroso/patologia
Regulação Enzimológica da Expressão Gênica
Glucose/metabolismo
Seres Humanos
Lipase/biossíntese
Metabolismo dos Lipídeos/genética
Lipogênese/genética
Lipólise/genética
Camundongos
Camundongos Transgênicos
Obesidade/metabolismo
Obesidade/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fatty Acids); 0 (Srebf1 protein, mouse); 0 (Sterol Regulatory Element Binding Protein 1); EC 3.1.1.3 (Lipase); EC 3.1.1.3 (hepatic lipase, human); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180102
[Lr] Data última revisão:
180102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171216
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189834


  8 / 2038 MEDLINE  
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[PMID]:27773935
[Au] Autor:Meng Q; Duan XP; Wang CY; Liu ZH; Sun PY; Huo XK; Sun HJ; Peng JY; Liu KX
[Ad] Endereço:Department of Clinical Pharmacology, College of Pharmacy, Dalian Medical University, Dalian 116044, China.
[Ti] Título:Alisol B 23-acetate protects against non-alcoholic steatohepatitis in mice via farnesoid X receptor activation.
[So] Source:Acta Pharmacol Sin;38(1):69-79, 2017 Jan.
[Is] ISSN:1745-7254
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Alisol B 23-acetate (AB23A) is a natural triterpenoid isolated from the traditional Chinese medicine rhizoma alismatis, which exhibits a number of pharmacological activities, including anti-hepatitis virus, anti-cancer and antibacterial effects. In this study we examined whether AB23A protected against non-alcoholic steatohepatitis (NASH) in mice, and the mechanisms underlying the protective effects. NASH was induced in mice fed a methionine and choline-deficient (MCD) diet for 4 weeks. The mice were simultaneously treated with AB23A (15, 30, and 60 mg·kg ·d , ig) for 4 weeks. On the last day, blood samples and livers were collected. Serum liver functional enzymes, inflammatoru markers were assessed. The livers were histologically examined using H&E, Oil Red O, Masson's trichrome and Sirius Red staining. Mouse primary hepatocytes were used for in vitro experiments. The mechanisms underlying AB23A protection were analyzed using siRNA, qRT-PCR, and Western blot assays. AB23A treatment significantly and dose-dependently decreased the elevated levels of serum ALT and AST in MCD diet-fed mice. Furthermore, AB23A treatment significantly reduced hepatic triglyceride accumulation, inflammatory cell infiltration and hepatic fibrosis in the mice. AB23A-induced decreases in serum and hepatic lipids were related to decreased hepatic lipogenesis through decreasing hepatic levels of SREBP-1c, FAS, ACC1 and SCD1 and increased lipid metabolism via inducing PPARα, CPT1α, ACADS and LPL. The reduction in inflammatory cell infiltration corresponded to deceased serum levels of mKC and MCP-1 and decreased hepatic gene expression of MCP-1 and VCAM-1. The reduction in hepatic fibrosis was correlated with decreased hepatic gene expression of fibrosis markers. The protective effects of AB23A were FXR-dependent, because treatment with the FXR agonist CDCA mimicked AB23A-induced hepato-protection in the mice, whereas co-administration of FXR antagonist guggulsterone abrogated AB23A-induced hepato-protection. In mouse primary hepatocytes, FXR gene silencing abrogated AB23A-induced changes in gene expression of Apo C-II, CPT1α, ACADS and LPL. AB23A produces protective effects against NASH in mice via FXR activation.
[Mh] Termos MeSH primário: Colestenonas/farmacologia
Hepatopatia Gordurosa não Alcoólica/prevenção & controle
Receptores Citoplasmáticos e Nucleares/agonistas
[Mh] Termos MeSH secundário: Animais
Ácido Quenodesoxicólico/farmacologia
Colestenonas/antagonistas & inibidores
Deficiência de Colina
Relação Dose-Resposta a Droga
Fibrose/patologia
Expressão Gênica/efeitos dos fármacos
Hepatócitos/metabolismo
Metabolismo dos Lipídeos/efeitos dos fármacos
Lipogênese/efeitos dos fármacos
Fígado/enzimologia
Fígado/metabolismo
Fígado/patologia
Masculino
Metionina/deficiência
Camundongos
Pregnenodionas/farmacologia
Cultura Primária de Células
Substâncias Protetoras/farmacologia
Receptores Citoplasmáticos e Nucleares/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cholestenones); 0 (Pregnenediones); 0 (Protective Agents); 0 (Receptors, Cytoplasmic and Nuclear); 0 (alisol B 23-acetate); 0 (farnesoid X-activated receptor); 0GEI24LG0J (Chenodeoxycholic Acid); A4PW148END (pregna-4,17-diene-3,16-dione); AE28F7PNPL (Methionine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:180101
[Lr] Data última revisão:
180101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE
[do] DOI:10.1038/aps.2016.119


  9 / 2038 MEDLINE  
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[PMID]:29232555
[Au] Autor:Guri Y; Colombi M; Dazert E; Hindupur SK; Roszik J; Moes S; Jenoe P; Heim MH; Riezman I; Riezman H; Hall MN
[Ad] Endereço:Biozentrum, University of Basel, 4056 Basel, Switzerland.
[Ti] Título:mTORC2 Promotes Tumorigenesis via Lipid Synthesis.
[So] Source:Cancer Cell;32(6):807-823.e12, 2017 Dec 11.
[Is] ISSN:1878-3686
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Dysregulated mammalian target of rapamycin (mTOR) promotes cancer, but underlying mechanisms are poorly understood. We describe an mTOR-driven mouse model that displays hepatosteatosis progressing to hepatocellular carcinoma (HCC). Longitudinal proteomic, lipidomics, and metabolomic analyses revealed that hepatic mTORC2 promotes de novo fatty acid and lipid synthesis, leading to steatosis and tumor development. In particular, mTORC2 stimulated sphingolipid (glucosylceramide) and glycerophospholipid (cardiolipin) synthesis. Inhibition of fatty acid or sphingolipid synthesis prevented tumor development, indicating a causal effect in tumorigenesis. Increased levels of cardiolipin were associated with tubular mitochondria and enhanced oxidative phosphorylation. Furthermore, increased lipogenesis correlated with elevated mTORC2 activity and HCC in human patients. Thus, mTORC2 promotes cancer via formation of lipids essential for growth and energy production.
[Mh] Termos MeSH primário: Carcinogênese/metabolismo
Carcinoma Hepatocelular/metabolismo
Fígado Gorduroso/metabolismo
Lipogênese/fisiologia
Neoplasias Hepáticas/metabolismo
Alvo Mecanístico do Complexo 2 de Rapamicina/metabolismo
[Mh] Termos MeSH secundário: Animais
Carcinoma Hepatocelular/etiologia
Transformação Celular Neoplásica/metabolismo
Fígado Gorduroso/complicações
Seres Humanos
Lipídeos/biossíntese
Neoplasias Hepáticas/etiologia
Camundongos
Camundongos Knockout
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Lipids); EC 2.7.11.1 (Mechanistic Target of Rapamycin Complex 2)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171220
[Lr] Data última revisão:
171220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171213
[St] Status:MEDLINE


  10 / 2038 MEDLINE  
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[PMID]:29173222
[Au] Autor:Lavandera J; Gerstner CD; Saín J; Fariña AC; González MA; Bernal CA
[Ad] Endereço:1Cátedra de Bromatología y Nutrición, Facultad de Bioquímica y Ciencias Biológicas,Universidad Nacional del Litoral,Ciudad Universitaria, Paraje el Pozo S/N, C.C. 242 (C.P. 3000),Santa Fe,Argentina.
[Ti] Título:Maternal conjugated linoleic acid modulates TAG metabolism in adult rat offspring.
[So] Source:Br J Nutr;118(11):906-913, 2017 Dec.
[Is] ISSN:1475-2662
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Conjugated linoleic acid (CLA) might regulate the lipid depots in liver and adipose tissue. As there is an association between maternal nutrition, fat depots and risk of offspring chronic disease, the aim was to investigate the effect of maternal CLA consumption on TAG regulation and some inflammatory parameters in adult male rat offspring receiving or not receiving CLA. Female Wistar rats were fed control (C) or CLA-supplemented (1 %, w/w) diets during 4 weeks before and throughout pregnancy and lactation. After weaning, male offspring of CLA rats were fed C or CLA diets (CLA/C and CLA/CLA groups, respectively), whereas C male rat offspring were fed a C diet (C/C group) for 9 weeks. Serum TAG levels were increased in the CLA/CLA and CLA/C groups, associated with a reduction of lipoprotein lipase activity and weights of adipose tissue. The liver TAG levels were decreased in the CLA/CLA group, related to a significant reduction of fatty acid synthase (FAS), acetyl-CoA carboxylase (ACC) and glucose-6-phosphate dehydrogenase enzyme activities, as well as to the mRNA levels of FAS, ACC, stearoyl-CoA desaturase-1 and sterol regulatory element-binding protein-1c. Even though normal TAG levels were found in the liver of CLA/C rats, a reduction of lipogenesis was also observed. Thus, these results demonstrated a programming effect of CLA on the lipid metabolic pathways leading to a preventive effect on the TAG accretion in adipose tissue and the liver of male rat offspring. This knowledge could be important to develop some dietary strategies leading to a reduced incidence of obesity and fatty acid liver disease in humans.
[Mh] Termos MeSH primário: Fenômenos Fisiológicos da Nutrição Animal
Ácidos Linoleicos Conjugados/farmacologia
Triglicerídeos/sangue
Triglicerídeos/metabolismo
[Mh] Termos MeSH secundário: Acetil-CoA Carboxilase/genética
Acetil-CoA Carboxilase/metabolismo
Tecido Adiposo Branco/efeitos dos fármacos
Tecido Adiposo Branco/metabolismo
Animais
Dieta
Gorduras na Dieta/administração & dosagem
Gorduras na Dieta/sangue
Ácido Graxo Sintases/genética
Ácido Graxo Sintases/metabolismo
Ácidos Graxos/sangue
Feminino
Glucosefosfato Desidrogenase/genética
Glucosefosfato Desidrogenase/metabolismo
Lipogênese/efeitos dos fármacos
Fígado/efeitos dos fármacos
Fígado/metabolismo
Masculino
Fenômenos Fisiológicos da Nutrição Materna
Gravidez
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Ratos
Ratos Wistar
Estearoil-CoA Dessaturase/genética
Estearoil-CoA Dessaturase/metabolismo
Proteína de Ligação a Elemento Regulador de Esterol 1/genética
Proteína de Ligação a Elemento Regulador de Esterol 1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Dietary Fats); 0 (Fatty Acids); 0 (Linoleic Acids, Conjugated); 0 (RNA, Messenger); 0 (Sterol Regulatory Element Binding Protein 1); 0 (Triglycerides); EC 1.1.1.49 (Glucosephosphate Dehydrogenase); EC 1.14.19.1 (Stearoyl-CoA Desaturase); EC 2.3.1.85 (Fatty Acid Synthases); EC 6.4.1.2 (Acetyl-CoA Carboxylase)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171218
[Lr] Data última revisão:
171218
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE
[do] DOI:10.1017/S0007114517003002



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