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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


  2 / 2704 MEDLINE  
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[PMID]:29185736
[Au] Autor:You SK; Joo YC; Kang DH; Shin SK; Hyeon JE; Woo HM; Um Y; Park C; Han SO
[Ad] Endereço:Department of Biotechnology, Korea University , Seoul 02841, Republic of Korea.
[Ti] Título:Enhancing Fatty Acid Production of Saccharomyces cerevisiae as an Animal Feed Supplement.
[So] Source:J Agric Food Chem;65(50):11029-11035, 2017 Dec 20.
[Is] ISSN:1520-5118
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Saccharomyces cerevisiae is used for edible purposes, such as human food or as an animal feed supplement. Fatty acids are also beneficial as feed supplements, but S. cerevisiae produces small amounts of fatty acids. In this study, we enhanced fatty acid production of S. cerevisiae by overexpressing acetyl-CoA carboxylase, thioesterase, and malic enzyme associated with fatty acid metabolism. The enhanced strain pAMT showed 2.4-fold higher fatty acids than the wild-type strain. To further increase the fatty acids, various nitrogen sources were analyzed and calcium nitrate was selected as an optimal nitrogen source for fatty acid production. By concentration optimization, 672 mg/L of fatty acids was produced, which was 4.7-fold higher than wild-type strain. These results complement the low level fatty acid production and make it possible to obtain the benefits of fatty acids as an animal feed supplement while, simultaneously, maintaining the advantages of S. cerevisiae.
[Mh] Termos MeSH primário: Ração Animal/análise
Bovinos/metabolismo
Suplementos Nutricionais/análise
Ácidos Graxos/biossíntese
Saccharomyces cerevisiae/metabolismo
[Mh] Termos MeSH secundário: Acetil-CoA Carboxilase/genética
Acetil-CoA Carboxilase/metabolismo
Animais
Bovinos/crescimento & desenvolvimento
Engenharia Metabólica
Saccharomyces cerevisiae/enzimologia
Saccharomyces cerevisiae/genética
Proteínas de Saccharomyces cerevisiae/genética
Proteínas de Saccharomyces cerevisiae/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fatty Acids); 0 (Saccharomyces cerevisiae Proteins); EC 6.4.1.2 (Acetyl-CoA Carboxylase)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180110
[Lr] Data última revisão:
180110
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171130
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jafc.7b04485


  3 / 2704 MEDLINE  
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[PMID]:29175208
[Au] Autor:Tanaka Y; Kume S; Maeda S; Osawa N; Takeda N; Chin-Kanasaki M; Isshiki K; Ugi S; Oshima I; Uzu T; Maegawa H; Araki SI
[Ad] Endereço:Department of Medicine, Shiga University of Medical Science, Otsu, Japan.
[Ti] Título:Overexpression of acetyl CoA carboxylase ß exacerbates podocyte injury in the kidney of streptozotocin-induced diabetic mice.
[So] Source:Biochem Biophys Res Commun;495(1):1115-1121, 2018 01 01.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A single nucleotide polymorphism (SNP) within the acetyl CoA carboxylase (ACC) ß gene (ACACB), rs2268388, has been shown to be associated with susceptibility to development of proteinuria in patients with type 2 diabetes. To investigate the biological roles of ACCß in the pathogenesis of diabetic nephropathy, we examined the effects of overexpression of ACACB using podocyte-specific ACACB-transgenic mice or ACACB-overexpressing murine podocytes. Podocyte-specific ACACB-transgenic mice or littermate mice were treated with streptozotocin (STZ) to induce diabetes, and 12 weeks after induction of diabetes, we examined the expression of podocyte markers to evaluate the degree of podocyte injury in these mice. We also examined the effects of ACCß on podocyte injury in ACACB- or LacZ-overexpressing murine podocytes. Podocyte-specific ACACB overexpression did not cause visible podocyte injury in non-diabetic mice. In STZ-induced diabetic mice, ACACB-transgenic mice showed a significant increase in urinary albumin excretion, accompanied by decreased synaptopodin expression and podocin mislocalization in podocytes, compared with wild-type mice. In cultured murine podocytes, overexpression of ACACB significantly decreased synaptopodin expression and reorganized stress fibers under high glucose conditions, but not in normal glucose conditions. The decrease of synaptopodin expression and reorganized stress fibers observed in ACACB overexpressing cells cultured under high glucose conditions was reversed by a treatment of 5-aminoimidazole-4-carboxamide-1-beta-4-ribofuranoside (AICAR), activator of AMP-activated protein kinase (AMPK). The excess of ACCß might contribute to exacerbation of podocyte injury in the kidney of an animal model for diabetes mellitus, and the AMPK/ACCß pathway may be a novel therapeutic target for the prevention of diabetes-related podocyte injury.
[Mh] Termos MeSH primário: Acetil-CoA Carboxilase/metabolismo
Nefropatias Diabéticas/enzimologia
Nefropatias Diabéticas/patologia
Podócitos/enzimologia
Podócitos/patologia
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Regulação Enzimológica da Expressão Gênica
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
EC 6.4.1.2 (Acacb protein, mouse); EC 6.4.1.2 (Acetyl-CoA Carboxylase)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180105
[Lr] Data última revisão:
180105
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE


  4 / 2704 MEDLINE  
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[PMID]:29173234
[Au] Autor:López-Oliva ME; Garcimartin A; Muñoz-Martínez E
[Ad] Endereço:1Sección Departamental de Fisiología, Facultad de Farmacia,Universidad Complutense de Madrid,28040 Madrid,Spain.
[Ti] Título:Dietary α-lactalbumin induced fatty liver by enhancing nuclear liver X receptor αß/sterol regulatory element-binding protein-1c/PPARγ expression and minimising PPARα/carnitine palmitoyltransferase-1 expression and AMP-activated protein kinase α phosphorylation associated with atherogenic dyslipidaemia, insulin resistance and oxidative stress in Balb/c mice.
[So] Source:Br J Nutr;118(11):914-929, 2017 Dec.
[Is] ISSN:1475-2662
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The effect and the role played by dietary α-lactalbumin (α-LAC) on hepatic fat metabolism are yet to be fully elucidated. We reported previously that α-LAC intake induced atherogenic dyslipidaemia in Balb/c mice. The aim of the present study was to investigate if this atherogenic effect could be due to a possible α-LAC-induced hepatic steatosis. We examine the ability of dietary α-LAC to induce liver steatosis, identifying the molecular mechanisms underlying hepatic lipid metabolism in association with the lipid profile, peripheral insulin resistance (IR) and changes in the hepatic oxidative environment. Male Balb/c mice (n 6) were fed with diets containing either chow or 14 % α-LAC for 4 weeks. The α-LAC-fed mice developed abdominal adiposity and IR. Moderate liver steatosis with increased TAG and NEFA contents was correlated with atherogenic dyslipidaemia. There was increased nuclear expression of liver X receptor αß (LXRαß), sterol regulatory element-binding protein-1c (SREBP-1c) and PPARγ transcription factors and of the cytosolic enzymes acetyl-CoA carboxylase 1 (ACC1) and fatty acid synthase involved in the hepatic de novo lipogenesis. The opposite was found for the nuclear receptor PPARα and the mitochondrial enzyme carnitine palmitoyltransferase-1 (CPT-1), leading to reduced fatty acid ß-oxidation (FAO). These changes were associated with a significant decrease in both p-Thr172-AMP-activated protein kinase α (AMPKα) (inactivation) and p-Ser79-ACC1 (activation) and with a more oxidative liver environment increasing lipid peroxidation and protein oxidation and reducing GSH:GSSG ratio in the α-LAC-fed mice. In conclusion, 4 weeks of 14 % α-LAC feeding induced liver steatosis associated with atherogenic dyslipidaemia, IR and oxidative stress by enhancing nuclear LXRαß/SREBP-1c/PPARγ expression and diminishing PPARα/CPT-1 expression and AMPKα phosphorylation shifting the hepatic FAO toward fatty acid synthesis in Balb/c mice.
[Mh] Termos MeSH primário: Carnitina O-Palmitoiltransferase/metabolismo
Fígado Gorduroso/metabolismo
Receptores X do Fígado/metabolismo
PPAR alfa/metabolismo
PPAR gama/metabolismo
Proteína de Ligação a Elemento Regulador de Esterol 1/metabolismo
[Mh] Termos MeSH secundário: Proteínas Quinases Ativadas por AMP/genética
Proteínas Quinases Ativadas por AMP/metabolismo
Acetil-CoA Carboxilase/genética
Acetil-CoA Carboxilase/metabolismo
Animais
Aterosclerose/diagnóstico
Aterosclerose/etiologia
Aterosclerose/genética
Carnitina O-Palmitoiltransferase/genética
Dislipidemias/diagnóstico
Dislipidemias/etiologia
Dislipidemias/genética
Fígado Gorduroso/induzido quimicamente
Fígado Gorduroso/genética
Resistência à Insulina
Lactalbumina/efeitos adversos
Peroxidação de Lipídeos/efeitos dos fármacos
Fígado/efeitos dos fármacos
Fígado/metabolismo
Receptores X do Fígado/genética
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Estresse Oxidativo
PPAR alfa/genética
PPAR gama/genética
Fosforilação
Proteína de Ligação a Elemento Regulador de Esterol 1/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Liver X Receptors); 0 (PPAR alpha); 0 (PPAR gamma); 0 (Srebf1 protein, mouse); 0 (Sterol Regulatory Element Binding Protein 1); 9013-90-5 (Lactalbumin); EC 2.3.1.21 (CPT1B protein, mouse); EC 2.3.1.21 (Carnitine O-Palmitoyltransferase); EC 2.7.11.31 (AMP-Activated Protein Kinases); EC 6.4.1.2 (ACC1 protein, mouse); 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/S000711451700232X


  5 / 2704 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


  6 / 2704 MEDLINE  
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[PMID]:29056104
[Au] Autor:Cuthbert CE; Foster JE; Ramdath DD
[Ad] Endereço:1Department of Pre-Clinical Sciences, Faculty of Medical Sciences,The University of the West Indies,St. Augustine,Trinidad and Tobago, West Indies.
[Ti] Título:A maternal high-fat, high-sucrose diet alters insulin sensitivity and expression of insulin signalling and lipid metabolism genes and proteins in male rat offspring: effect of folic acid supplementation.
[So] Source:Br J Nutr;118(8):580-588, 2017 Oct.
[Is] ISSN:1475-2662
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:A maternal high-fat, high-sucrose (HFS) diet alters offspring glucose and lipid homoeostasis through unknown mechanisms and may be modulated by folic acid. We investigated the effect of a maternal HFS diet on glucose homoeostasis, expression of genes and proteins associated with insulin signalling and lipid metabolism and the effect of prenatal folic acid supplementation (HFS/F) in male rat offspring. Pregnant Sprague-Dawley rats were randomly fed control (CON), HFS or HFS/F diets. Offspring were weaned on CON; at postnatal day 70, fasting plasma insulin and glucose and liver and skeletal muscle gene and protein expression were measured. Treatment effects were assessed by one-way ANOVA. Maternal HFS diet induced higher fasting glucose in offspring v. HFS/F (P=0·027) and down-regulation (P<0·05) of genes coding for v-Akt murine thymoma viral oncogene homolog 2, resistin and v-Raf-1 murine leukaemia viral oncogene homolog 1 (Raf1) in offspring skeletal muscle and acetyl-CoA carboxylase (Acaca), fatty acid synthase and phosphatidylinositol-4,5-biphosphate 3-kinase, catalytic subunit ß in offspring liver. Skeletal muscle neuropeptide Y and hepatic Kruppel-like factor 10 were up-regulated in HFS v. CON offspring (P<0·05). Compared with CON, Acaca and Raf1 protein expression levels were significantly lower in HFS offspring. Maternal HFS induced higher homoeostasis model of assessment index of insulin resistance v. CON (P=0·030) and HFS/F was associated with higher insulin (P=0·016) and lower glucose (P=0·025). Maternal HFS diet alters offspring insulin sensitivity and de novo hepatic lipogenesis via altered gene and protein expression, which appears to be potentiated by folate supplementation.
[Mh] Termos MeSH primário: Dieta Hiperlipídica
Resistência à Insulina
Insulina/sangue
Metabolismo dos Lipídeos
Fenômenos Fisiológicos da Nutrição Materna
[Mh] Termos MeSH secundário: Acetil-CoA Carboxilase/genética
Acetil-CoA Carboxilase/metabolismo
Animais
Animais Recém-Nascidos
Glicemia/metabolismo
Regulação para Baixo
Ácido Graxo Sintases/genética
Ácido Graxo Sintases/metabolismo
Feminino
Ácido Fólico/administração & dosagem
Fígado/metabolismo
Masculino
Fosfotransferases (Aceptor do Grupo Álcool)/genética
Fosfotransferases (Aceptor do Grupo Álcool)/metabolismo
Gravidez
Efeitos Tardios da Exposição Pré-Natal
Proteínas Proto-Oncogênicas c-akt/genética
Proteínas Proto-Oncogênicas c-akt/metabolismo
Proteínas Proto-Oncogênicas c-raf/genética
Proteínas Proto-Oncogênicas c-raf/metabolismo
Ratos
Ratos Sprague-Dawley
Resistina/genética
Resistina/metabolismo
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Insulin); 0 (Resistin); 0 (Retn protein, rat); 935E97BOY8 (Folic Acid); EC 2.3.1.85 (Fatty Acid Synthases); EC 2.7.1.- (Phosphotransferases (Alcohol Group Acceptor)); EC 2.7.1.- (phosphatidylinositol 4,5-biphosphate kinase); EC 2.7.11.1 (Akt2 protein, rat); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 2.7.11.1 (Proto-Oncogene Proteins c-raf); EC 2.7.11.1 (Raf1 protein, rat); EC 6.4.1.2 (Acetyl-CoA Carboxylase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171024
[St] Status:MEDLINE
[do] DOI:10.1017/S0007114517002501


  7 / 2704 MEDLINE  
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[PMID]:28946929
[Au] Autor:Chen GH; Hogstrand C; Luo Z; Zhang DG; Ling SC; Wu K
[Ad] Endereço:1Key Laboratory of Freshwater Animal Breeding,Ministry of Agriculture of P.R.C.,Fishery College,Huazhong Agricultural University,Wuhan 430070,People's Republic of China.
[Ti] Título:Dietary zinc addition influenced zinc and lipid deposition in the fore- and mid-intestine of juvenile yellow catfish Pelteobagrus fulvidraco.
[So] Source:Br J Nutr;118(8):570-579, 2017 Oct.
[Is] ISSN:1475-2662
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The present study explored the mechanisms of dietary Zn influencing Zn and lipid deposition in the fore- and mid- intestine in yellow catfish Pelteobagrus fulvidraco, and investigated whether the mechanism was intestinal-region dependent. For this purpose, yellow catfish were fed three diets containing Zn levels of 8·83, 19·20 and 146·65 mg Zn/kg, respectively. Growth performance, intestinal TAG and Zn contents as well as activities and mRNA expression of enzymes and genes involved in Zn transport and lipid metabolism in the fore- and mid-intestine were analysed. Dietary Zn increased Zn accumulation as well as activities of Cu-, Zn-superoxide dismutase and ATPase in the fore- and mid-intestine. In the fore-intestine, dietary Zn up-regulated mRNA levels of ZnT1, ZnT5, ZnT7, metallothionein (MT) and metal response element-binding transcription factor-1 (MTF-1), but down-regulated mRNA levels of ZIP4 and ZIP5. In the mid-intestine, dietary Zn up-regulated mRNA levels of ZnT1, ZnT5, ZnT7, MT and MTF-1, but down-regulated mRNA levels of ZIP4 and ZIP5. Dietary Zn reduced TAG content, down-regulated activities of 6-phosphogluconate dehydrogenase (6PGD), glucose-6-phosphate dehydrogenase (G6PD), malic enzyme (ME) and fatty acid synthase (FAS) activities, and reduced mRNA levels of 6PGD, G6PD, FAS, PPARγ and sterol-regulator element-binding protein (SREBP-1), but up-regulated mRNA levels of carnitine palmitoyltransferase IA, hormone-sensitive lipase (HSLa), adipose TAG lipase (ATGL) and PPARα in the fore-intestine. In the mid-intestine, dietary Zn reduced TAG content, activities of G6PD, ME, isocitrate dehydrogenase and FAS, down-regulated mRNA levels of 6PGD, G6PD, FAS, acetyl-CoA carboxylase a, PPARγ and SREBP-1, but up-regulated mRNA expression of HSLa, ATGL and PPARγ. The reduction in TAG content following Zn addition was attributable to reduced lipogenesis and increased lipolysis, and similar regulatory mechanisms were observed between the fore- and mid-intestine.
[Mh] Termos MeSH primário: Peixes-Gato/metabolismo
Intestinos/efeitos dos fármacos
Metabolismo dos Lipídeos/efeitos dos fármacos
Zinco/administração & dosagem
[Mh] Termos MeSH secundário: Acetil-CoA Carboxilase/genética
Acetil-CoA Carboxilase/metabolismo
Ração Animal/análise
Animais
Carnitina O-Palmitoiltransferase/genética
Carnitina O-Palmitoiltransferase/metabolismo
Dieta/veterinária
Regulação para Baixo
Regulação da Expressão Gênica
Glucosefosfato Desidrogenase/genética
Glucosefosfato Desidrogenase/metabolismo
Intestinos/metabolismo
Malato Desidrogenase/genética
Malato Desidrogenase/metabolismo
PPAR alfa/genética
PPAR alfa/metabolismo
PPAR gama/genética
PPAR gama/metabolismo
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Esterol Esterase/genética
Esterol Esterase/metabolismo
Proteína de Ligação a Elemento Regulador de Esterol 1/genética
Proteína de Ligação a Elemento Regulador de Esterol 1/metabolismo
Superóxido Dismutase/genética
Superóxido Dismutase/metabolismo
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (PPAR alpha); 0 (PPAR gamma); 0 (RNA, Messenger); 0 (Sterol Regulatory Element Binding Protein 1); EC 1.1.1.37 (Malate Dehydrogenase); EC 1.1.1.39 (malate dehydrogenase (decarboxylating)); EC 1.1.1.49 (Glucosephosphate Dehydrogenase); EC 1.15.1.1 (Superoxide Dismutase); EC 2.3.1.21 (Carnitine O-Palmitoyltransferase); EC 3.1.1.13 (Sterol Esterase); EC 6.4.1.2 (Acetyl-CoA Carboxylase); J41CSQ7QDS (Zinc)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170927
[St] Status:MEDLINE
[do] DOI:10.1017/S0007114517002446


  8 / 2704 MEDLINE  
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[PMID]:28938451
[Au] Autor:Lewis JE; Samms RJ; Cooper S; Luckett JC; Perkins AC; Dunbar JD; Smith DP; Emmerson PJ; Adams AC; Ebling FJP; Tsintzas K
[Ad] Endereço:School of Life Sciences, University of Nottingham, Queen's Medical Centre, Nottingham NG7 2UH, United Kingdom.
[Ti] Título:Antibody-Mediated Targeting of the FGFR1c Isoform Increases Glucose Uptake in White and Brown Adipose Tissue in Male Mice.
[So] Source:Endocrinology;158(10):3090-3096, 2017 Oct 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The increased prevalence of obesity and its cardiometabolic implications demonstrates the imperative to identify novel therapeutic targets able to effect meaningful metabolic changes in this population. Antibody-mediated targeting of fibroblast growth factor receptor 1c isoform (FGFR1c) has been shown to ameliorate hyperglycemia and protect from diet- and genetically-induced obesity in rodents and nonhuman primates. However, it is currently unknown which tissue(s) contribute to this glucose-lowering effect. Thus, to elucidate this effect, we treated euglycemic mice with H7, a monoclonal antibody that selectively targets FGFR1c, and used whole-body positron emission computed tomography with a glucose tracer (18F-fluorodeoxyglucose). Treatment with H7 increased basal glucose uptake in white adipose tissue (WAT), brown adipose tissue (BAT), the brain, and liver but reduced it in the quadriceps muscles. Consequentially, blood glucose was significantly reduced in response to treatment. Under insulin-stimulated conditions, the effects of H7 were maintained in WAT, BAT, liver, and muscle. Treatment with H7 decreased triglyceride (TG) content and increased adipose TG lipase content in white adipose tissue, while increasing activation of acetyl coenzyme A carboxylase, suggesting futile cycling of TGs, albeit favoring net hydrolysis. We demonstrated, in vitro, this is a direct effect of treatment in adipose tissue, as basal cellular respiration and glucose uptake were increased in response to treatment. Taken together, these data suggest that antibody-mediated targeting of FGFR1c exerts its powerful glucose-lowering efficacy primarily due to increased glucose uptake in adipose tissue.
[Mh] Termos MeSH primário: Tecido Adiposo Marrom/metabolismo
Tecido Adiposo Branco/metabolismo
Anticorpos Monoclonais/administração & dosagem
Receptor Tipo 1 de Fator de Crescimento de Fibroblastos/antagonistas & inibidores
[Mh] Termos MeSH secundário: Acetil-CoA Carboxilase/metabolismo
Animais
Anticorpos Monoclonais/uso terapêutico
Glicemia/análise
Encéfalo/efeitos dos fármacos
Encéfalo/metabolismo
Ativação Enzimática/efeitos dos fármacos
Glucose/metabolismo
Insulina/farmacologia
Lipase/análise
Fígado/efeitos dos fármacos
Fígado/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Músculo Esquelético/efeitos dos fármacos
Músculo Esquelético/metabolismo
Obesidade/metabolismo
Isoformas de Proteínas
Receptor Tipo 1 de Fator de Crescimento de Fibroblastos/imunologia
Triglicerídeos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Blood Glucose); 0 (Insulin); 0 (Protein Isoforms); 0 (Triglycerides); EC 2.7.10.1 (FGFR1 protein, human); EC 2.7.10.1 (Receptor, Fibroblast Growth Factor, Type 1); EC 3.1.1.3 (Lipase); EC 6.4.1.2 (Acetyl-CoA Carboxylase); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171114
[Lr] Data última revisão:
171114
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170923
[St] Status:MEDLINE
[do] DOI:10.1210/en.2017-00591


  9 / 2704 MEDLINE  
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[PMID]:28880122
[Au] Autor:Kinnunen SME; Mänttäri SK; Saarela SYO
[Ti] Título:Expression of AMPK, SIRT1, and ACC Differs between Winter- and Summer-Acclimatized Djungarian Hamsters.
[So] Source:Physiol Biochem Zool;90(6):605-612, 2017 Nov/Dec.
[Is] ISSN:1537-5293
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The wintering strategy of the Djungarian hamster (Phodopus sungorus) includes a naturally occurring decrease in food intake and body mass. Our aim was to investigate the conceivable role of the metabolic regulators, AMP-activated protein kinase (AMPK) and sirtuin 1 (SIRT1), in the seasonal adaptation of the Djungarian hamster. In addition, a rate-limiting enzyme in fatty acid synthesis and oxidation, acetyl CoA carboxylase (ACC), was studied. Relative protein expressions and phosphorylated forms (pAMPK and pACC) were determined by Western blot from subcutaneous white adipose tissues (sWAT), abdominal white adipose tissues (aWAT), interscapular brown adipose tissues (iBAT), skeletal muscle, and hypothalamus of winter- and summer-acclimatized hamsters. The winter group had higher AMPK expression in sWAT, aWAT, and iBAT, but the relative amount of phosphorylated protein (pAMPK/AMPK ratio) was lower in these tissues. Furthermore, ACC expression was higher in sWAT and iBAT of the winter animals. pACC (inactive form) levels were higher in all adipose tissues, yet a lower pACC/ACC ratio was detected in iBAT of the winter hamsters. Muscle AMPK expression was lower but pAMPK/AMPK ratio higher in the winter group. SIRT1 expression was higher in muscle and all adipose tissues of the winter hamsters. Hypothalamic protein expressions did not differ between the groups. Higher expressions of AMPK, ACC, and SIRT1 in WAT and iBAT of the winter hamsters suggest a role in the regulation of lipid reserves and increased thermogenic capacity characteristic to the winter-adapted Djungarian hamsters.
[Mh] Termos MeSH primário: Proteínas Quinases Ativadas por AMP/metabolismo
Aclimatação/fisiologia
Acetil-CoA Carboxilase/metabolismo
Phodopus/fisiologia
Estações do Ano
Sirtuína 1/metabolismo
[Mh] Termos MeSH secundário: Proteínas Quinases Ativadas por AMP/genética
Acetil-CoA Carboxilase/genética
Animais
Cricetinae
Feminino
Regulação da Expressão Gênica/fisiologia
Masculino
Sirtuína 1/genética
Temperatura Ambiente
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 2.7.11.31 (AMP-Activated Protein Kinases); EC 3.5.1.- (Sirtuin 1); EC 6.4.1.2 (Acetyl-CoA Carboxylase)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170908
[St] Status:MEDLINE
[do] DOI:10.1086/694295


  10 / 2704 MEDLINE  
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[PMID]:28876239
[Au] Autor:Yamada KD; Kunishima N; Matsuura Y; Nakai K; Naitow H; Fukasawa Y; Tomii K
[Ad] Endereço:Artificial Intelligence Research Center, National Institute of Advanced Industrial Science and Technology (AIST), 2-4-7 Aomi, Koto-ku, Tokyo 135-0064, Japan.
[Ti] Título:Designing better diffracting crystals of biotin carboxyl carrier protein from Pyrococcus horikoshii by a mutation based on the crystal-packing propensity of amino acids.
[So] Source:Acta Crystallogr D Struct Biol;73(Pt 9):757-766, 2017 Sep 01.
[Is] ISSN:2059-7983
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:An alternative rational approach to improve protein crystals by using single-site mutation of surface residues is proposed based on the results of a statistical analysis using a compiled data set of 918 independent crystal structures, thereby reflecting not only the entropic effect but also other effects upon protein crystallization. This analysis reveals a clear difference in the crystal-packing propensity of amino acids depending on the secondary-structural class. To verify this result, a systematic crystallization experiment was performed with the biotin carboxyl carrier protein from Pyrococcus horikoshii OT3 (PhBCCP). Six single-site mutations were examined: Ala138 on the surface of a ß-sheet was mutated to Ile, Tyr, Arg, Gln, Val and Lys. In agreement with prediction, it was observed that the two mutants (A138I and A138Y) harbouring the residues with the highest crystal-packing propensities for ß-sheet at position 138 provided better crystallization scores relative to those of other constructs, including the wild type, and that the crystal-packing propensity for ß-sheet provided the best correlation with the ratio of obtaining crystals. Two new crystal forms of these mutants were obtained that diffracted to high resolution, generating novel packing interfaces with the mutated residues (Ile/Tyr). The mutations introduced did not affect the overall structures, indicating that a ß-sheet can accommodate a successful mutation if it is carefully selected so as to avoid intramolecular steric hindrance. A significant negative correlation between the ratio of obtaining amorphous precipitate and the crystal-packing propensity was also found.
[Mh] Termos MeSH primário: Acetil-CoA Carboxilase/química
Proteínas Arqueais/química
Pyrococcus horikoshii/química
[Mh] Termos MeSH secundário: Acetil-CoA Carboxilase/genética
Aminoácidos/química
Aminoácidos/genética
Proteínas Arqueais/genética
Cristalografia por Raios X
Ácido Graxo Sintase Tipo II/química
Ácido Graxo Sintase Tipo II/genética
Modelos Moleculares
Mutagênese Sítio-Dirigida
Conformação Proteica
Estrutura Secundária de Proteína
Pyrococcus horikoshii/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amino Acids); 0 (Archaeal Proteins); EC 6.- (Fatty Acid Synthase, Type II); EC 6.4.1.2 (Acetyl-CoA Carboxylase); EC 6.4.1.2 (biotin carboxyl carrier protein)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170914
[Lr] Data última revisão:
170914
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170907
[St] Status:MEDLINE
[do] DOI:10.1107/S2059798317010932



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