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  1 / 454 MEDLINE  
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[PMID]:28841613
[Au] Autor:Ma J; Yao Y; Wang J; Dong Z; Zhou T; Lu F; Liao Y; Gao J
[Ad] Endereço:Guangzhou, Guangdong, People's Republic of China From the Department of Plastic and Cosmetic Surgery, Nanfang Hospital, Southern Medical University.
[Ti] Título:Dedifferentiated Adipocytes Promote Adipose Tissue Generation within an External Suspension Device.
[So] Source:Plast Reconstr Surg;140(3):525-536, 2017 Sep.
[Is] ISSN:1529-4242
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Mature adipocytes can dedifferentiate into fibroblast-like cells in vitro and acquire proliferation and redifferentiation/transdifferentiation abilities. A soft-tissue expander can induce adipocyte dedifferentiation in vivo. This study combined a tissue expander and an external suspension device to generate a large volume of adipose tissue. METHODS: A soft-tissue expander was implanted beneath the dorsal adipose flaps of rabbits. After 7 days of expansion, the expander was removed and an external suspension device was applied. Samples were collected at various time points, and morphologic, histologic, immunohistochemical, and gene expression analyses were conducted. A silicone sheet was implanted as a control. RESULTS: After 7 days of expansion, the adipose flap was much thinner. Hematoxylin and eosin and whole-mount staining revealed that adipocytes became smaller (p < 0.05) and some contained multilocular lipid droplets. The number of Ki67 cells increased (p < 0.01), adipokine expression decreased (p < 0.01), and octamer-binding transcription factor 4 expression increased (p < 0.01). After the external suspension device was applied, the normalized volume of adipose flaps was much larger in the expanded group than in the control group (p < 0.05). The expanded group also exhibited more proliferating cells, a larger vascularized area, and higher adipokine expression (p < 0.05). CONCLUSION: Dedifferentiated adipocytes in adipose flaps can participate in adipose tissue generation as seed cells and increase the volume of adipose tissue.
[Mh] Termos MeSH primário: Adipócitos/citologia
Tecido Adiposo/citologia
Desdiferenciação Celular
Expansão de Tecido/métodos
[Mh] Termos MeSH secundário: Animais
Proliferação Celular
Transdiferenciação Celular
Citocinas/metabolismo
Seres Humanos
Antígeno Ki-67/metabolismo
Masculino
Modelos Animais
Perilipina-1/metabolismo
Coelhos
Dispositivos para Expansão de Tecidos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Ki-67 Antigen); 0 (Perilipin-1)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170918
[Lr] Data última revisão:
170918
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170826
[St] Status:MEDLINE
[do] DOI:10.1097/PRS.0000000000003601


  2 / 454 MEDLINE  
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[PMID]:28801319
[Au] Autor:Gao Q; Binns DD; Kinch LN; Grishin NV; Ortiz N; Chen X; Goodman JM
[Ad] Endereço:Department of Pharmacology, University of Texas Southwestern Medical School, Dallas, TX.
[Ti] Título:Pet10p is a yeast perilipin that stabilizes lipid droplets and promotes their assembly.
[So] Source:J Cell Biol;216(10):3199-3217, 2017 Oct 02.
[Is] ISSN:1540-8140
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Pet10p is a yeast lipid droplet protein of unknown function. We show that it binds specifically to and is stabilized by droplets containing triacylglycerol (TG). Droplets isolated from cells with a deletion strongly aggregate, appear fragile, and fuse in vivo when cells are cultured in oleic acid. Pet10p binds early to nascent droplets, and their rate of appearance is decreased in Moreover, Pet10p functionally interacts with the endoplasmic reticulum droplet assembly factors seipin and Fit2 to maintain proper droplet morphology. The activity of Dga1p, a diacylglycerol acyltransferase, and TG accumulation were both 30-35% lower in the absence of Pet10p. Pet10p contains a PAT domain, a defining property of perilipins, which was not previously known to exist in yeast. We propose that the core functions of Pet10p and other perilipins extend beyond protection from lipases and include the preservation of droplet integrity as well as collaboration with seipin and Fit2 in droplet assembly and maintenance.
[Mh] Termos MeSH primário: Proteínas de Transporte de Cátions/metabolismo
Subunidades gama da Proteína de Ligação ao GTP/metabolismo
Glicoproteínas/metabolismo
Gotículas Lipídicas/metabolismo
Perilipina-1/metabolismo
Proteínas de Saccharomyces cerevisiae/metabolismo
Saccharomyces cerevisiae/metabolismo
[Mh] Termos MeSH secundário: Proteínas de Transporte de Cátions/genética
Subunidades gama da Proteína de Ligação ao GTP/genética
Glicoproteínas/genética
Perilipina-1/genética
Domínios Proteicos
Saccharomyces cerevisiae/genética
Proteínas de Saccharomyces cerevisiae/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cation Transport Proteins); 0 (FIT2 protein, S cerevisiae); 0 (GTP-Binding Protein gamma Subunits); 0 (Glycoproteins); 0 (Perilipin-1); 0 (Saccharomyces cerevisiae Proteins); 0 (seipin protein, S cerevisiae)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171007
[Lr] Data última revisão:
171007
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170813
[St] Status:MEDLINE
[do] DOI:10.1083/jcb.201610013


  3 / 454 MEDLINE  
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[PMID]:28579235
[Au] Autor:Liu P; Huang G; Cao Z; Xie Q; Wei T; Huang C; Li Q; Sun M; Shen W; Gao P
[Ad] Endereço:State Key Laboratory of Medical Genomics, Shanghai Key Laboratory of Hypertension, Department of Hypertension Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200025, China; Shanghai Jiaotong University Affiliated Sixth People's Hospital, Shanghai 200233, China.
[Ti] Título:Haematopoietic TLR4 deletion attenuates perivascular brown adipose tissue inflammation in atherosclerotic mice.
[So] Source:Biochim Biophys Acta;1862(9):946-957, 2017 09.
[Is] ISSN:0006-3002
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: To investigate whether haematopoietic TLR4 deletion attenuates perivascular brown adipose tissue inflammation in atherosclerotic mice. METHODS AND RESULTS: Experiments were performed using irradiated LDL receptor-deficient (LDLR ) mice with marrow from either TLR4-deficient (TLR4 ) or age-matched wild-type (WT) mice. After 12 weeks of being fed a high-cholesterol diet, TLR4 →LDLR mice developed fewer atherosclerotic lesions in the aorta compared to WT→LDLR mice. This effect was associated with an increase in multilocular lipid droplets and mitochondria in perivascular adipose tissue (PVAT). Immunofluorescence analysis confirmed that there was an increase in capillary density and M2 macrophage infiltration, accompanied by a decrease in tumour necrosis factor (TNF)-α expression in the localized PVAT of TLR4 →LDLR mice. In vitro studies indicated that bone marrow-derived macrophages (BMDMs) from WT mice demonstrated an M1-like phenotype and expression of inflammatory cytokines induced by palmitate. These effects were attenuated in BMDMs isolated from TLR4 mice. Furthermore, brown adipocytes incubated with conditioned medium (CM) derived from palmitate-treated BMDMs, exhibited larger and more unilocular lipid droplets, and reduced expression of brown adipocyte-specific markers and perilipin-1 compared to those observed in brown adipocytes exposed to CM from palmitate-treated BMDMs of TLR4 mice. This decreased potency was primarily due to TNF-α, as demonstrated by the capacity of the TNF-α neutralizing antibody to reverse these effects. CONCLUSIONS: These results suggest that haematopoietic-specific deletion of TLR4 promotes PVAT homeostasis, which is involved in reducing macrophage-induced TNF-α secretion and increasing mitochondrial biogenesis in brown adipocytes.
[Mh] Termos MeSH primário: Tecido Adiposo Marrom/metabolismo
Aterosclerose/metabolismo
Inflamação/metabolismo
Receptor 4 Toll-Like/metabolismo
[Mh] Termos MeSH secundário: Animais
Biomarcadores/metabolismo
Medula Óssea/metabolismo
Gotículas Lipídicas/metabolismo
Macrófagos/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Perilipina-1/metabolismo
Receptores de LDL/metabolismo
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biomarkers); 0 (Perilipin-1); 0 (Receptors, LDL); 0 (Tlr4 protein, mouse); 0 (Toll-Like Receptor 4); 0 (Tumor Necrosis Factor-alpha)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170606
[St] Status:MEDLINE


  4 / 454 MEDLINE  
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[PMID]:28429532
[Au] Autor:Natori Y; Nasui M; Kihara-Negishi F
[Ad] Endereço:Department of Life and Health Sciences, School of Pharma-Sciences, Teikyo University, 2-11-1 Kaga, Itabashi-ku, Tokyo, 173-8605, Japan.
[Ti] Título:Neu1 sialidase interacts with perilipin 1 on lipid droplets and inhibits lipolysis in 3T3-L1 adipocytes.
[So] Source:Genes Cells;22(5):485-492, 2017 May.
[Is] ISSN:1365-2443
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Fatty acids are stored within adipocytes in lipid droplets (LDs) as triacylglycerol (TG), which is converted to free fatty acid (FFA) and glycerol via lipolysis. Increased plasma FFA levels in obesity are associated with several clinical conditions. We previously found that Neu1 activity is aberrant in the epididymal fat and liver of obese and diabetic mice. Here, we examined involvement of Neu1 in lipolysis in 3T3-L1 adipocytes. Small interfering RNA against Neu1 was introduced into adipocytes, and glycerol concentrations were measured in the culture medium. We then assessed the effects of Neu1 knockdown on lipolytic protein expression and phosphorylation, as well as interactions between perilipin 1 (Plin1) and hormone-sensitive lipase (HSL) after isoproterenol (IS) stimulation. Interactions between Neu1 and Plin1 were analyzed by immunoprecipitation and immunofluorescent imaging using adipocytes transfected with pCMV6-mNeu1-myc-DYKDDDDK (mNeu1DDK). Neu1 knockdown increased glycerol concentrations in culture media and Plin1 phosphorylation in whole lysates of IS-stimulated cells. Neu1 knockdown increased interaction between Plin1 and HSL after IS stimulation whereas that between Neu1 and Plin1 on LD observed under basal conditions was lost. These results suggest that Neu1 inhibits lipolysis induced by ß-adrenergic stimulation in adipocytes via interactions with Plin1 on LD.
[Mh] Termos MeSH primário: Adipócitos/metabolismo
Gotículas Lipídicas/metabolismo
Lipólise
Neuraminidase/metabolismo
Perilipina-1/metabolismo
[Mh] Termos MeSH secundário: Células 3T3
Adipócitos/efeitos dos fármacos
Agonistas Adrenérgicos beta/farmacologia
Animais
Camundongos
Neuraminidase/genética
Ligação Proteica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adrenergic beta-Agonists); 0 (Perilipin-1); 0 (Plin1 protein, mouse); EC 3.2.1.18 (Neu1 protein, mouse); EC 3.2.1.18 (Neuraminidase)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170911
[Lr] Data última revisão:
170911
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170422
[St] Status:MEDLINE
[do] DOI:10.1111/gtc.12490


  5 / 454 MEDLINE  
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[PMID]:28348166
[Au] Autor:Boutant M; Kulkarni SS; Joffraud M; Ratajczak J; Valera-Alberni M; Combe R; Zorzano A; Cantó C
[Ad] Endereço:Nestlé Institute of Health Sciences, Lausanne, Switzerland.
[Ti] Título:Mfn2 is critical for brown adipose tissue thermogenic function.
[So] Source:EMBO J;36(11):1543-1558, 2017 Jun 01.
[Is] ISSN:1460-2075
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Mitochondrial fusion and fission events, collectively known as mitochondrial dynamics, act as quality control mechanisms to ensure mitochondrial function and fine-tune cellular bioenergetics. Defective mitofusin 2 (Mfn2) expression and enhanced mitochondrial fission in skeletal muscle are hallmarks of insulin-resistant states. Interestingly, Mfn2 is highly expressed in brown adipose tissue (BAT), yet its role remains unexplored. Using adipose-specific Mfn2 knockout (Mfn2-adKO) mice, we demonstrate that Mfn2, but not Mfn1, deficiency in BAT leads to a profound BAT dysfunction, associated with impaired respiratory capacity and a blunted response to adrenergic stimuli. Importantly, Mfn2 directly interacts with perilipin 1, facilitating the interaction between the mitochondria and the lipid droplet in response to adrenergic stimulation. Surprisingly, Mfn2-adKO mice were protected from high-fat diet-induced insulin resistance and hepatic steatosis. Altogether, these results demonstrate that Mfn2 is a mediator of mitochondria to lipid droplet interactions, influencing lipolytic processes and whole-body energy homeostasis.
[Mh] Termos MeSH primário: Tecido Adiposo Marrom/metabolismo
GTP Fosfo-Hidrolases/metabolismo
Mitocôndrias/metabolismo
Termogênese
[Mh] Termos MeSH secundário: Animais
GTP Fosfo-Hidrolases/deficiência
Camundongos
Camundongos Knockout
Perilipina-1/metabolismo
Ligação Proteica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Perilipin-1); 0 (Plin1 protein, mouse); EC 3.6.1.- (GTP Phosphohydrolases); EC 3.6.1.- (Mfn2 protein, mouse)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170713
[Lr] Data última revisão:
170713
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170329
[St] Status:MEDLINE
[do] DOI:10.15252/embj.201694914


  6 / 454 MEDLINE  
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[PMID]:28292967
[Au] Autor:Kuo T; Chen TC; Lee RA; Nguyen NHT; Broughton AE; Zhang D; Wang JC
[Ad] Endereço:Endocrinology Graduate Program, University of California, Berkeley, Berkeley, CA.
[Ti] Título:Pik3r1 Is Required for Glucocorticoid-Induced Perilipin 1 Phosphorylation in Lipid Droplet for Adipocyte Lipolysis.
[So] Source:Diabetes;66(6):1601-1610, 2017 Jun.
[Is] ISSN:1939-327X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Glucocorticoids promote lipolysis in white adipose tissue (WAT) to adapt to energy demands under stress, whereas superfluous lipolysis causes metabolic disorders, including dyslipidemia and hepatic steatosis. Glucocorticoid-induced lipolysis requires the phosphorylation of cytosolic hormone-sensitive lipase (HSL) and perilipin 1 (Plin1) in the lipid droplet by protein kinase A (PKA). We previously identified Pik3r1 (also called ) as a glucocorticoid receptor target gene. Here, we found that glucocorticoids increased HSL phosphorylation, but not Plin1 phosphorylation, in adipose tissue-specific -null (AKO) mice. Furthermore, in lipid droplets, the phosphorylation of HSL and Plin1 and the levels of catalytic and regulatory subunits of PKA were increased by glucocorticoids in wild-type mice. However, these effects were attenuated in AKO mice. In agreement with reduced WAT lipolysis, glucocorticoid- initiated hepatic steatosis and hypertriglyceridemia were improved in AKO mice. Our data demonstrated a novel role of Pik3r1 that was independent of the regulatory function of phosphoinositide 3-kinase in mediating the metabolic action of glucocorticoids. Thus, the inhibition of Pik3r1 in adipocytes could alleviate lipid disorders caused by excess glucocorticoid exposure.
[Mh] Termos MeSH primário: Adipócitos/metabolismo
Classe Ia de Fosfatidilinositol 3-Quinase/genética
Gotículas Lipídicas/metabolismo
Lipólise
Perilipina-1/metabolismo
[Mh] Termos MeSH secundário: Adipócitos/efeitos dos fármacos
Tecido Adiposo Branco/metabolismo
Animais
Western Blotting
Dexametasona/farmacologia
Ácidos Graxos não Esterificados/metabolismo
Técnicas de Silenciamento de Genes
Glucocorticoides/farmacologia
Insulina/metabolismo
Gotículas Lipídicas/efeitos dos fármacos
Camundongos
Perilipina-1/efeitos dos fármacos
Fosfatidilinositol 3-Quinases/genética
Fosforilação/efeitos dos fármacos
Fosforilação/genética
Reação em Cadeia da Polimerase em Tempo Real
Esterol Esterase/efeitos dos fármacos
Esterol Esterase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fatty Acids, Nonesterified); 0 (Glucocorticoids); 0 (Insulin); 0 (Perilipin-1); 0 (Plin1 protein, mouse); 7S5I7G3JQL (Dexamethasone); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.1.137 (Class Ia Phosphatidylinositol 3-Kinase); EC 2.7.1.137 (Pik3r1 protein, mouse); EC 3.1.1.13 (Sterol Esterase)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170822
[Lr] Data última revisão:
170822
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170316
[St] Status:MEDLINE
[do] DOI:10.2337/db16-0831


  7 / 454 MEDLINE  
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[PMID]:28260008
[Au] Autor:Xia W; Zhou Y; Wang L; Wang L; Liu X; Lin Y; Zhou Q; Huang J; Liu L
[Ad] Endereço:Department of Endocrinology, Fujian Medical University Union Hospital, Fuzhou, Fujian 350001, P.R. China.
[Ti] Título:Tauroursodeoxycholic acid inhibits TNF-α-induced lipolysis in 3T3-L1 adipocytes via the IRE-JNK-perilipin-A signaling pathway.
[So] Source:Mol Med Rep;15(4):1753-1758, 2017 Apr.
[Is] ISSN:1791-3004
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:The present study investigated the effects of tauroursodeoxycholic acid (TUDCA) on the lipolytic action of tumor necrosis factor (TNF)-α in 3T3-L1 adipocytes. Following treatment with TNF­α, cell viability was determined by MTT assay to select the optimum concentration and duration of TNF­α treatment in 3T3­L1 adipocytes. Intracellular lipid droplet dispersion and glycerin content in culture media were determined to evaluate the effect of TUDCA on TNF­α­induced lipolysis in 3T3­L1 adipocytes. Western blotting was performed to detect protein expression levels of perilipin­A and protein markers of endoplasmic reticulum stress: Immunoglobulin­binding protein (BiP), inositol­requiring enzyme (IRE), c­Jun N­terminal kinase (JNK), phosphorylated (p)­IRE and p­JNK. Following treatment with 50 ng/ml TNF­α for 24 h, glycerin content increased significantly and lipid droplets were dispersed. Glycerin content was reduced significantly and dispersal of lipid droplets reduced following pretreatment of 3T3­L1 adipocytes with 1 mmol/l TUDCA. TNF­α additionally activated the expression of BiP, p­IRE and p­JNK in a time­dependent manner; following pretreatment of 3T3­L1 adipocytes with 1 mmol/l TUDCA, the expression levels of these three proteins decreased. Therefore, TUDCA may inhibit TNF-α-induced lipolysis in 3T3­L1 adipocytes and reduce production of free fatty acids. Its underlying molecular mechanisms are potentially associated with the inhibition of activation of the IRE­JNK signaling pathway, which influences perilipin-A expression levels.
[Mh] Termos MeSH primário: Adipócitos/metabolismo
Endorribonucleases/metabolismo
Proteínas Quinases JNK Ativadas por Mitógeno/metabolismo
Lipólise/efeitos dos fármacos
Perilipina-1/metabolismo
Proteínas Serina-Treonina Quinases/metabolismo
Transdução de Sinais/efeitos dos fármacos
Ácido Tauroquenodesoxicólico/farmacologia
Fator de Necrose Tumoral alfa/farmacologia
[Mh] Termos MeSH secundário: Células 3T3-L1
Adipócitos/efeitos dos fármacos
Animais
Biomarcadores/metabolismo
Sobrevivência Celular/efeitos dos fármacos
Estresse do Retículo Endoplasmático/efeitos dos fármacos
Gotículas Lipídicas/efeitos dos fármacos
Gotículas Lipídicas/metabolismo
Camundongos
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Perilipin-1); 0 (Tumor Necrosis Factor-alpha); 516-35-8 (Taurochenodeoxycholic Acid); 60EUX8MN5X (tauroursodeoxycholic acid); EC 2.7.11.1 (Ern1 protein, mouse); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases); EC 3.1.- (Endoribonucleases)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170522
[Lr] Data última revisão:
170522
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170306
[St] Status:MEDLINE
[do] DOI:10.3892/mmr.2017.6209


  8 / 454 MEDLINE  
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[PMID]:28219719
[Au] Autor:Haj-Yasein NN; Berg O; Jernerén F; Refsum H; Nebb HI; Dalen KT
[Ad] Endereço:Department of Nutrition, Institute of Basic Medical Sciences, University of Oslo, Norway.
[Ti] Título:Cysteine deprivation prevents induction of peroxisome proliferator-activated receptor gamma-2 and adipose differentiation of 3T3-L1 cells.
[So] Source:Biochim Biophys Acta;1862(6):623-635, 2017 06.
[Is] ISSN:0006-3002
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Plasma cysteine is strongly associated with body fat mass in human cohorts and diets low in cysteine prevents fat accumulation in mice. It is unclear if plasma cysteine affects fat development or if fat accumulation raises plasma cysteine. To determine if cysteine affects adipogenesis, we differentiated 3T3-L1 preadipocytes in medium with reduced cysteine. Cells incubated in media with 10-20µM cysteine exhibited reduced capacity to differentiate into triacylglycerol-storing mature adipocytes compared with cells incubated with 50µM cysteine. Low cysteine severely reduced expression of peroxisome proliferator-activated receptor gamma2 (Pparγ2) and its target genes perlipin1 (Plin1) and fatty acid binding protein-4 (Fabp4). Expression of stearoyl-CoA desaturase-1 (Scd1), known to be repressed with cysteine depletion, was also reduced with low cysteine. Medium depletion of the essential amino acids leucine, valine, and isoleucine had only a modest effect on adipocyte specific gene expression and differentiation. Stimulation with the PPARγ agonist BRL-49653 or addition of a hydrogen sulfide donor enhanced differentiation of 3T3-L1 cells cultured in low cysteine. This demonstrates that the ability to induce PPARγ expression is preserved when cells are cultured in low cysteine. It therefore appears that cysteine depletion inhibits adipogenesis by specifically affecting molecular pathways required for induction of PPARγ expression, rather than through a general reduction of global protein synthesis. In conclusion, we show that low extracellular cysteine reduces adipocyte differentiation by interfering with PPARγ2 and PPARγ target gene expression. Our results provide further evidence for the hypothesis that plasma cysteine is a casual determinant for body fat mass.
[Mh] Termos MeSH primário: Adipócitos/metabolismo
Diferenciação Celular/fisiologia
Cisteína/metabolismo
Proteínas de Ligação a Ácido Graxo/metabolismo
PPAR gama/metabolismo
Perilipina-1/metabolismo
Estearoil-CoA Dessaturase/metabolismo
[Mh] Termos MeSH secundário: Células 3T3-L1
Adipócitos/citologia
Animais
Cisteína/farmacologia
Proteínas de Ligação a Ácido Graxo/genética
Regulação da Expressão Gênica/fisiologia
Camundongos
PPAR gama/genética
Perilipina-1/genética
Estearoil-CoA Dessaturase/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Fabp4 protein, mouse); 0 (Fatty Acid-Binding Proteins); 0 (PPAR gamma); 0 (Perilipin-1); 0 (Plin1 protein, mouse); EC 1.14.19.1 (Scd1 protein, mouse); EC 1.14.19.1 (Stearoyl-CoA Desaturase); K848JZ4886 (Cysteine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170814
[Lr] Data última revisão:
170814
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170222
[St] Status:MEDLINE


  9 / 454 MEDLINE  
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[PMID]:28189761
[Au] Autor:Sandhu HS; Puri S; Sharma R; Sokhi J; Singh G; Matharoo K; Bhanwer A
[Ad] Endereço:Department of Human Genetics, Guru Nanak Dev University, Amritsar 143005, India; Centre for Stem Cell and Tissue Engineering, Panjab University, Chandigarh 160014, India.
[Ti] Título:Associating genetic variation at Perilipin 1, Complement Factor D and Adiponectin loci to the bone health status in North Indian population.
[So] Source:Gene;610:80-89, 2017 Apr 30.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Osteoporosis, the most common bone metabolic disease affecting nearly 200 million people worldwide is under the strong influence of genetic components. Simultaneously, adipogenesis and osteogenesis are two highly coordinated processes imperative for the maintenance of bone quality and quantity, where any perturbation leads to pathological conditions of obesity, osteopenia and osteoporosis. To delineate this adipogenic-osteogenic connection, a total of 254 cases (T-score<-1.0 SD) and 250 age, gender and ethnicity matched healthy controls (T-score≥-1.0 SD) were recruited from North India after analyzing bone health status employing quantitative ultrasound (QUS) bone densitometer. The genetic variants of Perilipin 1 (PLIN1), Complement Factor D (CFD) and Adiponectin (ADIPOQ) were genotyped using the PCR-RFLP/ARMS-PCR approach. Subjects with CC+CT (PLIN1 rs2304795) and CC+CG (CFD rs1683563) genotypes conferred nearly 1.54-1.87 fold increased risk towards bone deterioration. Predicted RNA secondary structures of rs2304795 corroborated the risk associated with wild type C allele. G allele carriers at the ADIPOQ locus (rs1501299) were more likely to have a lower bone health (1.57-fold). Haplotype analysis revealed the ADIPOQ variants rs1501299 and rs3774261 in slight linkage disequilibrium (LD), nonetheless G/G haplotype was associated with increased risk. 3-locus and 5-locus gene-gene interaction models revealed a greater likelihood of bone deterioration. In conclusion, certain variants of adipogenic genes might serve as potential biomarkers for determining the genetic predisposition towards bone loss in the North Indian population, further, emphasizing the role of impaired metabolism in bone health.
[Mh] Termos MeSH primário: Adipogenia
Adiponectina/genética
Osteogênese
Osteoporose/genética
Perilipina-1/genética
[Mh] Termos MeSH secundário: Adulto
Idoso
Osso e Ossos/metabolismo
Fator D do Complemento/genética
Epistasia Genética
Gorduras/metabolismo
Feminino
Seres Humanos
Índia/epidemiologia
Masculino
Meia-Idade
Conformação de Ácido Nucleico
Osteoporose/epidemiologia
Polimorfismo de Nucleotídeo Único
Estabilidade de RNA
RNA Mensageiro/química
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ADIPOQ protein, human); 0 (Adiponectin); 0 (Fats); 0 (PLIN1 protein, human); 0 (Perilipin-1); 0 (RNA, Messenger); EC 3.4.21.46 (Complement Factor D); EC 3.4.21.46 (complement factor D, human)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170315
[Lr] Data última revisão:
170315
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170213
[St] Status:MEDLINE


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[PMID]:28096119
[Au] Autor:Mojallal A; Shipkov C
[Ad] Endereço:From the Department of Plastic, Reconstructive, and Aesthetic Surgery, Croix Rousse Hospital, Hospices Civils de Lyon, Lyon, France. dr.mojallal@gmail.com.
[Ti] Título:Commentary on: Exposure to Tumescent Solution Significantly Increases Phosphorylation of Perilipin in Adipocytes.
[So] Source:Aesthet Surg J;37(2):248-249, 2017 02.
[Is] ISSN:1527-330X
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Adipócitos/metabolismo
Perilipina-1
[Mh] Termos MeSH secundário: Proteínas de Transporte/metabolismo
Seres Humanos
Lipólise
Fosfoproteínas/metabolismo
Fosforilação
[Pt] Tipo de publicação:JOURNAL ARTICLE; COMMENT
[Nm] Nome de substância:
0 (Carrier Proteins); 0 (Perilipin-1); 0 (Phosphoproteins)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170119
[St] Status:MEDLINE
[do] DOI:10.1093/asj/sjw213



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