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[PMID]:29311524
[Au] Autor:Ogata F; Obayashi M; Nagahashi E; Nakamura T; Kawasaki N
[Ad] Endereço:Faculty of Pharmacy, Kindai University.
[Ti] Título:Effects of Water Addition to Prevent Deterioration of Soybean Oil by Calcium Silicate Adsorbent.
[So] Source:J Oleo Sci;67(1):95-103, 2018.
[Is] ISSN:1347-3352
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:In this study, we prepared calcium silicate at different molar ratios (Ca:Si=1:3, 1:6, and 1:9 refer to CAS-30S, CAS-60S, and CAS-90S, respectively) with water addition. The adsorbent characteristics (specific surface area, pore volume, mean pore diameter, and elemental analysis) were measured and the effect of water addition on the adsorbent surface for the prevention of deterioration was evaluated. In addition, the deterioration of soybean oil (SO) subjected to heating and aeration was investigated based on the acid value (AV) and carbonyl value (CV). The specific surface area increased in the order CAS-60S (160.51 m /g) < CAS-30S (182.61 m /g) < CAS-90S (204.19 m /g). Deterioration of SO could be induced by heating and aeration with AV and CV of 1.4 mg/g and 102.9 µmol/g, respectively. The adsorbent (CAS-30S and CAS-90S) with water addition (25% and 50%) was found to decrease the AV, indicating that a small amount of water addition to adsorbent surface is important for the decreasing of AV. In addition, the correlation between the decrease in AV and the specific surface area is strongly positive (R value: 0.968). The adsorption mechanism is thought to involve interactions between the polar compounds (free fatty acids) in the SO (nonaqueous phase) and the water layer (containing calcium ions released from the adsorbent) on the adsorbent surface. In summary, the data obtained in this study provide useful information for preventing the deterioration of SO and prolonging the oil life cycle.
[Mh] Termos MeSH primário: Compostos de Cálcio/química
Silicatos/química
Óleo de Soja/química
Eliminação de Resíduos Líquidos
Poluição da Água/prevenção & controle
Água/química
[Mh] Termos MeSH secundário: Ácidos/análise
Adsorção
Cálcio
Ácidos Graxos não Esterificados
Temperatura Alta
Íons
Oxirredução
Propriedades de Superfície
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Acids); 0 (Calcium Compounds); 0 (Fatty Acids, Nonesterified); 0 (Ions); 0 (Silicates); 059QF0KO0R (Water); 8001-22-7 (Soybean Oil); S4255P4G5M (calcium silicate); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180110
[St] Status:MEDLINE
[do] DOI:10.5650/jos.ess17175


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[PMID]:29339725
[Au] Autor:Velazquez-Villegas LA; Perino A; Lemos V; Zietak M; Nomura M; Pols TWH; Schoonjans K
[Ad] Endereço:Institute of Bioengineering, Ecole Polytechnique Fédérale de Lausanne, CH-1015, Lausanne, Switzerland.
[Ti] Título:TGR5 signalling promotes mitochondrial fission and beige remodelling of white adipose tissue.
[So] Source:Nat Commun;9(1):245, 2018 01 16.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Remodelling of energy storing white fat into energy expending beige fat could be a promising strategy to reduce adiposity. Here, we show that the bile acid-responsive membrane receptor TGR5 mediates beiging of the subcutaneous white adipose tissue (scWAT) under multiple environmental cues including cold exposure and prolonged high-fat diet feeding. Moreover, administration of TGR5-selective bile acid mimetics to thermoneutral housed mice leads to the appearance of beige adipocyte markers and increases mitochondrial content in the scWAT of Tgr5 mice but not in their Tgr5 littermates. This phenotype is recapitulated in vitro in differentiated adipocytes, in which TGR5 activation increases free fatty acid availability through lipolysis, hence fuelling ß-oxidation and thermogenic activity. TGR5 signalling also induces mitochondrial fission through the ERK/DRP1 pathway, further improving mitochondrial respiration. Taken together, these data identify TGR5 as a druggable target to promote beiging with potential applications in the management of metabolic disorders.
[Mh] Termos MeSH primário: Tecido Adiposo Bege/metabolismo
Tecido Adiposo Branco/metabolismo
Dinâmica Mitocondrial
Receptores Acoplados a Proteínas-G/metabolismo
[Mh] Termos MeSH secundário: Células 3T3-L1
Adipócitos Bege/metabolismo
Adipócitos Brancos/metabolismo
Tecido Adiposo Bege/citologia
Tecido Adiposo Branco/citologia
Animais
Diferenciação Celular/genética
Linhagem Celular
Ácidos Graxos não Esterificados/metabolismo
Seres Humanos
Camundongos
Camundongos Knockout
Receptores Acoplados a Proteínas-G/genética
Transdução de Sinais/genética
Gordura Subcutânea/citologia
Gordura Subcutânea/metabolismo
Temperatura Ambiente
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Fatty Acids, Nonesterified); 0 (Gpbar1 protein, mouse); 0 (Receptors, G-Protein-Coupled)
[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:180118
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02068-0


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[PMID]:29240830
[Au] Autor:Warfel JD; Vandanmagsar B; Wicks SE; Zhang J; Noland RC; Mynatt RL
[Ad] Endereço:Pennington Biomedical Research Center, Louisiana State University, Baton Rouge, Louisiana, United States of America.
[Ti] Título:A low fat diet ameliorates pathology but retains beneficial effects associated with CPT1b knockout in skeletal muscle.
[So] Source:PLoS One;12(12):e0188850, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Inhibiting fatty acid oxidation is one approach to lowering glucose levels in diabetes. Skeletal muscle specific Carnitine Palmitoyltransferase 1b knockout mice (Cpt1bm-/-) comprise a model of impaired fat oxidation; and have decreased fat mass and enhanced glucose disposal and muscle oxidative capacity compared to controls. However, unfavorable effects occur relative to controls when Cpt1bm-/- mice are fed a 25% fat diet, including decreased activity and fat free mass and increased intramuscular lipid and serum myoglobin. In this study we explore if a low fat, high carbohydrate diet can ablate the unfavorable effects while maintaining the favorable phenotype in Cpt1bm-/- mice. Mice were fed either 10% fat (low fat) or 25% fat (chow) diet. Body composition was measured biweekly and indirect calorimetry was performed. Low fat diet abolishes the decreased activity, fat, and fat free mass seen in Cpt1bm-/- mice fed chow diet. Low fat diet also reduces serum myoglobin levels in Cpt1bm-/- mice and diminishes differences in IGF-1 seen between Cpt1bm-/- mice and control mice fed chow diet. Glucose tolerance tests reveal that glucose clearance is improved in Cpt1bm-/- mice relative to controls regardless of diet, and serum analysis shows increased levels of muscle derived FGF21. Electron microscopic analyses and measurements of mRNA transcripts show increased intramuscular lipids, FGF21, mitochondrial and oxidative capacity markers regardless of diet. The favorable metabolic phenotype of Cpt1bm-/- mice therefore remains consistent regardless of diet; and a combination of a low fat diet and pharmacological inhibition of CPT1b may offer remedies to reduce blood glucose.
[Mh] Termos MeSH primário: Carnitina O-Palmitoiltransferase/genética
Dieta com Restrição de Gorduras
Músculo Esquelético/patologia
[Mh] Termos MeSH secundário: Animais
Ingestão de Energia
Ácidos Graxos não Esterificados/metabolismo
Fator de Crescimento Insulin-Like I/metabolismo
Cetonas/metabolismo
Camundongos
Camundongos Knockout
Músculo Esquelético/metabolismo
Mioglobina/metabolismo
Ganho de Peso
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fatty Acids, Nonesterified); 0 (Ketones); 0 (Myoglobin); 67763-96-6 (Insulin-Like Growth Factor I); EC 2.3.1.21 (CPT1B protein, mouse); EC 2.3.1.21 (Carnitine O-Palmitoyltransferase)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171215
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188850


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[PMID]:29315384
[Au] Autor:Li S; Mbong EF; John DT; Terasaka T; Li D; Lawson MA
[Ad] Endereço:Department of Reproductive Medicine, University of California, San Diego, La Jolla, California.
[Ti] Título:Induction of Stress Signaling In Vitro and Suppression of Gonadotropin Secretion by Free Fatty Acids in Female Mouse Gonadotropes.
[So] Source:Endocrinology;159(2):1074-1087, 2018 02 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:An emerging body of evidence supports the concept that the pituitary is a site for integration of multiple physiological and metabolic signals that inform and modulate endocrine pathways. Multiple endocrine mediators of energy balance and adiposity are known to impinge on the neuroendocrine axis regulating reproduction. Observations in humans show that obesity is correlated with decreased gonadotropin secretion, and studies have also suggested that pituitary sensitivity to stimulation by gonadotropin-releasing hormone (GnRH) is decreased in obese individuals. Free fatty acids are a potential mediator of adiposity and energy balance, but their impact as an endocrine modulator of pituitary function has not been closely examined. We evaluated the impact of free fatty acids on a pituitary gonadotrope cell line and in primary pituitary cultures of female mice. We show that increasing physiologically relevant doses of the monounsaturated ω-9 fatty acid oleate induces cellular stress and increases production of reactive oxygen species in a mouse gonadotrope cell line. In contrast, the unsaturated ω-3 α-linolenic and ω-6 linoleic fatty acids do not have this effect. Additionally, oleate can activate immediate-early gene expression independent of GnRH stimulation but has a negative impact on GnRH induction and expression of the gonadotropin subunit gene Lhb. Further, oleate suppresses gonadotropin secretion in response to pulsatile stimulation by GnRH. These results indicate that free fatty acids can directly alter gonadotropin gene expression and secretion in response to GnRH and may provide a link between energy sensing and reproduction.
[Mh] Termos MeSH primário: Ácidos Graxos não Esterificados/farmacologia
Gonadotrofos/efeitos dos fármacos
Gonadotropinas/secreção
Estresse Fisiológico/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Feminino
Gonadotrofos/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Fatty Acids, Nonesterified); 0 (Gonadotropins)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180110
[St] Status:MEDLINE
[do] DOI:10.1210/en.2017-00638


  5 / 26198 MEDLINE  
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[PMID]:29037698
[Au] Autor:Liu M; Wei F; Lv X; Dong XY; Chen H
[Ad] Endereço:Oil Crops Research Institute of Chinese Academy of Agricultural Sciences, Key Laboratory of Oilseeds Processing of Ministry of Agriculture, Key Laboratory of Biology and Genetic Improvement of Oil Crops, Ministry of Agriculture, PR China; Hubei Key Laboratory of Lipid Chemistry and Nutrition, PR Chi
[Ti] Título:Rapid and sensitive detection of free fatty acids in edible oils based on chemical derivatization coupled with electrospray ionization tandem mass spectrometry.
[So] Source:Food Chem;242:338-344, 2018 Mar 01.
[Is] ISSN:0308-8146
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:In this study, a strategy based on chemical derivatization coupled with electrospray ionizationtandem quadrupole mass spectrometry (ESI-MS/MS) for rapid and sensitive detection of FFAs in edible oils was developed. A derivative reagent (N,N-diethyl-1,2-ethanediamine, DEEA) was employed to selectively label carboxyl groups of FFAs to form an amino compound with a tertiary amino group. The DEEA derivative products could lose a characteristic neutral loss fragment of 73Da in collision-induced dissociation (CID), which enabled to discriminate and analyze the DEEA derived FFAs with neutral loss scan (NLS 73Da)under the positive ion mode of mass spectrometry. The assay was linear over the concentration range 0.5-200nmol/L with satisfactory correlation coefficients (R ≥0.9942), whilst the limit of detection and quantitation were 0.1-0.3nmol/L and 0.3-1.0nmol/L, respectively. Finally, the established method was applied to determine dynamic FFA formation in seven types of edible oils subjected to a microwave heating treatment test.
[Mh] Termos MeSH primário: Ácidos Graxos não Esterificados/análise
Óleos Vegetais/análise
Espectrometria de Massas por Ionização por Electrospray/métodos
Espectrometria de Massas em Tandem/métodos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fatty Acids, Nonesterified); 0 (Plant Oils)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171018
[St] Status:MEDLINE


  6 / 26198 MEDLINE  
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[PMID]:29305863
[Au] Autor:Qu B; Gong K; Yang HS; Li YG; Jiang T; Zeng ZM; Cao ZR; Pan XM
[Ad] Endereço:Department of Orthopaedics, The First Affiliated Hospital of Chengdu Medical College, Chengdu, Sichuan Province, China; Center for Disease Control and Prevention of the Chengdu Military Command, Chengdu, Sichuan Province, China.
[Ti] Título:MiR-449 overexpression inhibits osteogenic differentiation of bone marrow mesenchymal stem cells via suppressing Sirt1/Fra-1 pathway in high glucose and free fatty acids microenvironment.
[So] Source:Biochem Biophys Res Commun;496(1):120-126, 2018 01 29.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Diabetic osteoporosis is a chronic complication caused by diabetes mellitus, and However, the exact mechanism of diabetes mellitus-induced osteoporosis is still unknown. In this study, we investigate the effect of miR-449 on osteogenic differentiation and its underlying mechanism in human bone marrow-derived mesenchymal stem cells (hBMSCs) with high glucose (HG) and free fatty acids (FFA) treatment. Results showed that after culturing for 14 days, high glucose (HG) and free fatty acids (FFA) treatment dramatically decreased mineralization of human bone marrow-derived mesenchymal stem cells (hBMSCs) compared with cells treated with osteogenic medium (OM) alone. We also found that miR-449 expression was up-regulated during osteogenic differentiation of hBMSCs with HG and FFA treatment. Moreover, during osteogenic differentiation of hBMSCs with HG and FFA treatment, miR-449 mimics notably decreased the alkaline phosphatase (ALP) activity and the mRNA and protein expression levels of runt-related transcription factor 2 (Runx2), ALP, collagen I, osteocalcin (OCN), and bone sialoprotein (BSP), which was remarkably increased by miR-449 inhibitors. Furthermore, miR-449 directly targets Sirt1 by binding to its 3'-UTR. Sirt1 overexpression reverses the suppressive effect of miR-449 mimics on Fra-1 mRNA and protein expression, which was also alleviated by Fra-1 overexpression. In addition, Fra-1 overexpression alleviates the inhibitory effect of miR-449 mimics on the ALP activity and the mRNA and protein of Runx2, collagen I, OCN and BSP. Taken together, our results indicated that miR-449 overexpression inhibited osteogenic differentiation of HG-FFA-treated hBMSCs through the Sirt1/Fra-1 signal pathway. It is conceivable that modulating miR-449 might provide a new therapy for intervention in diabetic osteoporosis.
[Mh] Termos MeSH primário: Ácidos Graxos não Esterificados/metabolismo
Glucose/metabolismo
Células Mesenquimais Estromais/citologia
Células Mesenquimais Estromais/fisiologia
Osteogênese/fisiologia
Proteínas Proto-Oncogênicas c-fos/metabolismo
Sirtuína 1/metabolismo
[Mh] Termos MeSH secundário: Diferenciação Celular/fisiologia
Células Cultivadas
Seres Humanos
Osteoblastos/citologia
Osteoblastos/fisiologia
Transdução de Sinais/fisiologia
Nicho de Células-Tronco/fisiologia
Regulação para Cima/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Fatty Acids, Nonesterified); 0 (Proto-Oncogene Proteins c-fos); 0 (fos-related antigen 1); EC 3.5.1.- (SIRT1 protein, human); EC 3.5.1.- (Sirtuin 1); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180215
[Lr] Data última revisão:
180215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180107
[St] Status:MEDLINE


  7 / 26198 MEDLINE  
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[PMID]:28450226
[Au] Autor:Hara A; Endo S; Matsunaga T; El-Kabbani O; Miura T; Nishinaka T; Terada T
[Ad] Endereço:Faculty of Engineering, Gifu University, Gifu 501-1193, Japan.
[Ti] Título:Human carbonyl reductase 1 participating in intestinal first-pass drug metabolism is inhibited by fatty acids and acyl-CoAs.
[So] Source:Biochem Pharmacol;138:185-192, 2017 08 15.
[Is] ISSN:1873-2968
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Human carbonyl reductase 1 (CBR1), a member of the short-chain dehydrogenase/reductase (SDR) superfamily, reduces a variety of carbonyl compounds including endogenous isatin, prostaglandin E and 4-oxo-2-nonenal. It is also a major non-cytochrome P450 enzyme in the phase I metabolism of carbonyl-containing drugs, and is highly expressed in the intestine. In this study, we found that long-chain fatty acids and their CoA ester derivatives inhibit CBR1. Among saturated fatty acids, myristic, palmitic and stearic acids were inhibitory, and stearic acid was the most potent (IC 9µM). Unsaturated fatty acids (oleic, elaidic, γ-linolenic and docosahexaenoic acids) and acyl-CoAs (palmitoyl-, stearoyl- and oleoyl-CoAs) were more potent inhibitors (IC 1.0-2.5µM), and showed high inhibitory selectivity to CBR1 over its isozyme CBR3 and other SDR superfamily enzymes (DCXR and DHRS4) with CBR activity. The inhibition by these fatty acids and acyl-CoAs was competitive with respect to the substrate, showing the K values of 0.49-1.2µM. Site-directed mutagenesis of the substrate-binding residues of CBR1 suggested that the interactions between the fatty acyl chain and the enzyme's Met141 and Trp229 are important for the inhibitory selectivity. We also examined CBR1 inhibition by oleic acid in cellular levels: The fatty acid effectively inhibited CBR1-mediated 4-oxo-2-nonenal metabolism in colon cancer DLD1 cells and increased sensitivity to doxorubicin in the drug-resistant gastric cancer MKN45 cells that highly express CBR1. The results suggest a possible new food-drug interaction through inhibition of CBR1-mediated intestinal first-pass drug metabolism by dietary fatty acids.
[Mh] Termos MeSH primário: Acil Coenzima A/metabolismo
Oxirredutases do Álcool/antagonistas & inibidores
Ácidos Graxos não Esterificados/metabolismo
Mucosa Intestinal/enzimologia
[Mh] Termos MeSH secundário: Oxirredutases do Álcool/genética
Oxirredutases do Álcool/metabolismo
Sítios de Ligação
Ligação Competitiva
Linhagem Celular Tumoral
Resistência a Medicamentos Antineoplásicos
Interações Alimento-Droga
Seres Humanos
Mutação
Ácido Mirístico/metabolismo
Proteínas de Neoplasias/antagonistas & inibidores
Proteínas de Neoplasias/metabolismo
Oxirredutases/antagonistas & inibidores
Oxirredutases/genética
Oxirredutases/metabolismo
Ácido Palmítico/metabolismo
Palmitoil Coenzima A/metabolismo
Proteínas Recombinantes/química
Proteínas Recombinantes/metabolismo
Ácidos Esteáricos/metabolismo
Desidrogenase do Álcool de Açúcar/antagonistas & inibidores
Desidrogenase do Álcool de Açúcar/genética
Desidrogenase do Álcool de Açúcar/metabolismo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Acyl Coenzyme A); 0 (Fatty Acids, Nonesterified); 0 (Neoplasm Proteins); 0 (Recombinant Proteins); 0 (Stearic Acids); 0I3V7S25AW (Myristic Acid); 1716-06-9 (oleoyl-coenzyme A); 1763-10-6 (Palmitoyl Coenzyme A); 2V16EO95H1 (Palmitic Acid); 362-66-3 (stearoyl-coenzyme A); 4ELV7Z65AP (stearic acid); EC 1.- (Oxidoreductases); EC 1.1.- (Alcohol Oxidoreductases); EC 1.1.- (Sugar Alcohol Dehydrogenases); EC 1.1.1.10 (L-xylulose reductase); EC 1.1.1.184 (CBR1 protein, human); EC 1.1.1.184 (CBR3 protein, human); EC 1.1.1.184 (DHRS4 protein, human)
[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:170429
[St] Status:MEDLINE


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[PMID]:27771766
[Au] Autor:Wagner R; Fritsche L; Heni M; Fehlert E; Stefan N; Staiger H; Häring HU; Fritsche A
[Ad] Endereço:Department of Internal Medicine IV, Division of Endocrinology, Diabetology, Nephrology, Vascular Disease and Clinical Chemistry, University Hospital of Tübingen, Tübingen, Germany.
[Ti] Título:A novel insulin sensitivity index particularly suitable to measure insulin sensitivity during gestation.
[So] Source:Acta Diabetol;53(6):1037-1044, 2016 Dec.
[Is] ISSN:1432-5233
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:AIMS: Insulin resistance underlies the etiology of both type 2 diabetes and gestational diabetes. In pregnancy, insulin resistance is also associated with an unfavorable metabolic programming of the fetus, potentially contributing to a higher risk of obesity and type 2 diabetes in the offspring. To assess insulin sensitivity, several methods based on glucose and insulin levels during a 75-g oral glucose tolerance test (OGTT) exist. It is unclear how they perform during pregnancy, where physiologically altered metabolism could introduce a bias. METHODS: In a cohort comprising 476 non-diabetic subjects undergoing OGTT and hyperinsulinemic-euglycemic clamp (HEC), we used cross-validation to develop an insulin sensitivity index also based on non-esterified fatty acids (NEFA) that could be more robust during pregnancy (NEFA-index). We tested commonly used OGTT-based indexes and the NEFA-index in a different cohort of 42 women during pregnancy and 1 year after delivery. RESULTS: The Matsuda and OGIS index failed to detect lower insulin sensitivity during pregnancy as compared to the follow-up OGTT 1 year after delivery (p > 0.09). The new NEFA-index incorporating BMI, plasma insulin and NEFA, but not glucose, clearly indicated lower insulin sensitivity during pregnancy (p < 0.0001). In the non-pregnant cohort, this NEFA-index correlated well with the gold-standard HEC-based insulin sensitivity index, and outperformed other tested indexes for the prediction of HEC-measured insulin resistance. CONCLUSIONS: This insulin/NEFA-based approach is feasible, robust, and could be consistently used to estimate insulin sensitivity also during pregnancy.
[Mh] Termos MeSH primário: Diabetes Mellitus Tipo 2
Diabetes Gestacional
Resistência à Insulina
Insulina/metabolismo
Gravidez em Diabéticas
[Mh] Termos MeSH secundário: Adulto
Glicemia/metabolismo
Diabetes Mellitus Tipo 2/sangue
Diabetes Mellitus Tipo 2/diagnóstico
Diabetes Gestacional/sangue
Diabetes Gestacional/diagnóstico
Ácidos Graxos não Esterificados/metabolismo
Estudos de Viabilidade
Feminino
Alemanha
Técnica Clamp de Glucose/métodos
Teste de Tolerância a Glucose/métodos
Seres Humanos
Gravidez
Gravidez em Diabéticas/sangue
Gravidez em Diabéticas/diagnóstico
Reprodutibilidade dos Testes
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Fatty Acids, Nonesterified); 0 (Insulin)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:180202
[Lr] Data última revisão:
180202
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE
[do] DOI:10.1007/s00592-016-0930-5


  9 / 26198 MEDLINE  
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[PMID]:29216638
[Au] Autor:Wu GY; Rui C; Chen JQ; Sho E; Zhan SS; Yuan XW; Ding YT
[Ad] Endereço:Department of Hepatobiliary Surgery, The Affiliated Drum Tower Hospital of Nanjing University Medical School, Nanjing, China.
[Ti] Título:MicroRNA-122 Inhibits Lipid Droplet Formation and Hepatic Triglyceride Accumulation via Yin Yang 1.
[So] Source:Cell Physiol Biochem;44(4):1651-1664, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: An increase in intracellular lipid droplet formation and hepatic triglyceride (TG) content usually results in nonalcoholic fatty liver disease. However, the mechanisms underlying the regulation of hepatic TG homeostasis remain unclear. METHODS: Oil red O staining and TG measurement were performed to determine the lipid content. miRNA expression was evaluated by quantitative PCR. A luciferase assay was performed to validate the regulation of Yin Yang 1 (YY1) by microRNA (miR)-122. The effects of miR-122 expression on YY1 and its mechanisms involving the farnesoid X receptor and small heterodimer partner (FXR-SHP) pathway were evaluated by quantitative PCR and Western blot analyses. RESULTS: miR-122 was downregulated in free fatty acid (FFA)-induced steatotic hepatocytes, and streptozotocin and high-fat diet (STZ-HFD) induced nonalcoholic steatohepatitis (NASH) in mice. Transfection of hepatocytes with miR-122 mimics before FFA induction inhibited lipid droplet formation and TG accumulation in vitro. These results were verified by overexpressing miR-122 in the livers of STZ-HFD-induced NASH mice. The 3'-untranslated region (3'UTR) of YY1 mRNA is predicted to contain an evolutionarily conserved miR-122 binding site. In silico searches, a luciferase reporter assay and quantitative PCR analysis confirmed that miR-122 directly bound to the YY1 3'UTR to negatively regulate YY1 mRNA in HepG2 and Huh7 cells. The (FXR-SHP) signaling axis, which is downstream of YY1, may play a key role in the mechanism of miR-122-regulated lipid homeostasis. YY1-FXR-SHP signaling, which is negatively regulated by FFA, was enhanced by miR-122 overexpression. This finding was also confirmed by overexpression of miR-122 in the livers of NASH mice. CONCLUSIONS: The present results indicate that miR-122 plays an important role in lipid (particularly TG) accumulation in the liver by reducing YY1 mRNA stability to upregulate FXR-SHP signaling.
[Mh] Termos MeSH primário: Gotículas Lipídicas/metabolismo
MicroRNAs/metabolismo
Triglicerídeos/metabolismo
Fator de Transcrição YY1/metabolismo
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas
Animais
Antagomirs/metabolismo
Sequência de Bases
Linhagem Celular Tumoral
Diabetes Mellitus Experimental/metabolismo
Diabetes Mellitus Experimental/patologia
Dieta Hiperlipídica
Modelos Animais de Doenças
Regulação para Baixo/efeitos dos fármacos
Ácidos Graxos não Esterificados/farmacologia
Proteína do X Frágil de Retardo Mental/genética
Proteína do X Frágil de Retardo Mental/metabolismo
Células Hep G2
Seres Humanos
Gotículas Lipídicas/efeitos dos fármacos
Fígado/metabolismo
Fígado/patologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
MicroRNAs/antagonistas & inibidores
MicroRNAs/genética
Hepatopatia Gordurosa não Alcoólica/metabolismo
Hepatopatia Gordurosa não Alcoólica/patologia
Receptores Citoplasmáticos e Nucleares/genética
Receptores Citoplasmáticos e Nucleares/metabolismo
Alinhamento de Sequência
Fator de Transcrição YY1/química
Fator de Transcrição YY1/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (Antagomirs); 0 (Fatty Acids, Nonesterified); 0 (MIRN122 microRNA, human); 0 (MicroRNAs); 0 (Receptors, Cytoplasmic and Nuclear); 0 (Triglycerides); 0 (YY1 Transcription Factor); 0 (nuclear receptor subfamily 0, group B, member 2); 139135-51-6 (Fragile X Mental Retardation Protein)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180118
[Lr] Data última revisão:
180118
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171208
[St] Status:MEDLINE
[do] DOI:10.1159/000485765


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[PMID]:29261667
[Au] Autor:Eldor R; Norton L; Fourcaudot M; Galindo C; DeFronzo RA; Abdul-Ghani M
[Ad] Endereço:Diabetes Unit, Institute for Metabolism, Endocrinology and Hypertension, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel.
[Ti] Título:Increased lipid availability for three days reduces whole body glucose uptake, impairs muscle mitochondrial function and initiates opposing effects on PGC-1α promoter methylation in healthy subjects.
[So] Source:PLoS One;12(12):e0188208, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:AIMS: FFA and FFA metabolites cause insulin resistance and impair beta cell function. The goal of our research was to examine whether elevation of plasma FFA impairs mitochondrial function and alters PGC-1α promoter methylation. METHODS: In this uncontrolled, change from baseline study design, insulin sensitivity and glucose-stimulated insulin secretion were measured in 9 normal glucose tolerant subjects before and after 3 day lipid infusion to elevate plasma FFA concentration. Vastus lateralis muscle biopsies were obtained and mitochondrial function, PGC-1α expression, and PGC-1α promoter methylation were quantitated. RESULTS: Increased plasma FFA (440±93 µmol/Lto 997±242 µM, p<0.001) decreased insulin-stimulated total glucose disposal (TGD) by 25% (p = 0.008), impaired suppression of endogenous glucose production (p = 0.01), and reduced mitochondrial ATP synthesis with complex 1 (34%, p<0.05) and complex 2 (30%, p<0.05) substrates. Lipid infusion had no effect on muscle PGC-1α RNA expression, total methylation or non-CpG methylation, but methylation of the alternative PGC-1α promoter decreased (1.30±0.30 to 0.84±0.15% methylated residues/patient•strand, p = 0.055). Within PGC-1α promoter there was demethylation of CpT residues (0.72±0.16 vs. 0.28±0.10 methylated residues/patient•strand) (p = 0.002), which was inversely correlated with PGC-1α mRNA expression (r = -0.94, p<0.0001) and ATP synthesis with complex 1 (r = -0.80, p<0.01) and complex 2 (r = -0.69, p<0.05) substrates. Lipid infusion increased DNMT-3B (methyltransferase associated with PGC-1α promoter non-CpG methylation) mRNA expression (0.87 ± 0.09 to 1.62 ± 0.22 arbitrary units, p = 0.005), which correlated inversely with CpT demethylation (r = 0.67, p<0.05). CONCLUSION/INTERPRETATION: Physiologic plasma FFA elevation in NGT individuals has opposing effects on PGC-1α non-CpG residue methylation (CpT demethylation and increased DNMT-3B expression), which is correlated with changes in PGC-1α expression and skeletal muscle mitochondrial function.
[Mh] Termos MeSH primário: Metilação de DNA
Glucose/metabolismo
Metabolismo dos Lipídeos
Mitocôndrias Musculares/fisiologia
Coativador 1-alfa do Receptor gama Ativado por Proliferador de Peroxissomo/genética
[Mh] Termos MeSH secundário: Trifosfato de Adenosina/biossíntese
Adulto
Ácidos Graxos não Esterificados/sangue
Feminino
Voluntários Saudáveis
Seres Humanos
Insulina/secreção
Resistência à Insulina
Masculino
Mitocôndrias Musculares/metabolismo
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fatty Acids, Nonesterified); 0 (Insulin); 0 (PPARGC1A protein, human); 0 (Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha); 8L70Q75FXE (Adenosine Triphosphate); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180116
[Lr] Data última revisão:
180116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171221
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188208



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