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We are analyzing https://link.springer.com/article/10.1007/s00125-006-0140-8.

Title:
Activation of liver X receptors promotes lipid accumulation but does not alter insulin action in human skeletal muscle cells | Diabetologia
Description:
Aims/hypothesis The aim of this study was to investigate the effects of liver X receptor (LXR) activation on lipid metabolism and insulin action in human skeletal muscle cells prepared from control subjects and from patients with type 2 diabetes. Subjects and methods Cultured myotubes were obtained from muscle biopsies of 11 lean, healthy control subjects and ten patients with type 2 diabetes. The mRNA levels of LXR isoforms and lipogenic genes were estimated by RT-quantitative PCR, and the effects of LXR agonists on insulin action were evaluated by assays of protein kinase B serine 473 phosphorylation and glycogen synthesis. Results Both LXRα and LXRβ were expressed in human skeletal muscle and adipose tissue and there was no difference in their mRNA abundance in tissues from patients with type 2 diabetes compared with control subjects. In cultured muscle cells, LXR activation by T0901317 strongly increased expression of the genes encoding lipogenic enzymes, including sterol regulatory element binding protein 1c, fatty acid synthase and stearoyl-CoA desaturase 1, and also promoted triglyceride accumulation in the presence of a high glucose concentration. Importantly, these effects on lipid metabolism did not affect protein kinase B activation by insulin. Furthermore, LXR agonists did not modify insulin action in muscle cells from patients with type 2 diabetes. Conclusions/interpretation These data suggest that LXR agonists may lead to increased utilisation of lipids and glucose in muscle cells without affecting the mechanism of action of insulin. However, the long-term consequences of triglyceride accumulation in muscle should be evaluated before the development of effective LXR-based therapeutic agents.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Science
  • Health & Fitness
  • Fitness & Wellness

Content Management System {📝}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 5,000,019 visitors per month in the current month.
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How Does Link.springer.com Make Money? {💸}

The income method remains a mystery to us.

Earning money isn't the goal of every website; some are designed to offer support or promote social causes. People have different reasons for creating websites. This might be one such reason. Link.springer.com might be earning cash quietly, but we haven't detected the monetization method.

Keywords {🔍}

insulin, muscle, lxr, cells, diabetes, human, skeletal, patients, glucose, type, expression, google, scholar, subjects, activation, myotubes, action, mrna, effect, srebpc, data, accumulation, fatty, control, lipid, protein, gene, fig, effects, levels, mmoll, genes, pkb, metabolism, adipose, tissue, acid, diabetic, liver, glycogen, receptor, agonists, condition, synthesis, expressed, sterol, regulatory, shown, differentiated, lxrα,

Topics {✒️}

long-chain acetyl-coas db/db diabetic mouse peroxisome proliferator-activated receptors quantitative real-time pcr parametric mann–whitney test rate-limiting enzyme catalysing mono-unsaturated fatty acids anti-phospho-ser473 antibody irs1/pi3kinase/pkb pathway real-time rt-qpcr fatty acid-induced lipotoxicity ten age-matched patients euglycaemic–hyperinsulinaemic clamp showed 4 amol/μg total rna insulin-dependent diabetes mellitus steady-state mrna levels dual luciferase assay fatty acid translocase transcription factor privacy choices/manage cookies adenovirus-mediated overexpression affect protein kinase insulin signalling pathway circulating fatty acid pkb signalling pathway saturated fatty acids fatty acid synthase stearoyl-coa desaturase 1 phosphorylated protein kinase human gene promoter total protein extract luciferase reporter constructs unsaturated fatty acids vastus lateralis muscle prl-cmv vector precursor protein levels rt-quantitative pcr fatty acid oxidation potential therapeutic agents de novo lipogenesis lxr-induced lipogenesis affected relative luciferase activity impaired glucose tolerance oxidise fatty acids fatty acid metabolism insulin-induced glycogen synthesis de la recherche faculté de médecine srebp1c promoter region lipogenesis-related genes

Schema {🗺️}

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         headline:Activation of liver X receptors promotes lipid accumulation but does not alter insulin action in human skeletal muscle cells
         description:The aim of this study was to investigate the effects of liver X receptor (LXR) activation on lipid metabolism and insulin action in human skeletal muscle cells prepared from control subjects and from patients with type 2 diabetes. Cultured myotubes were obtained from muscle biopsies of 11 lean, healthy control subjects and ten patients with type 2 diabetes. The mRNA levels of LXR isoforms and lipogenic genes were estimated by RT-quantitative PCR, and the effects of LXR agonists on insulin action were evaluated by assays of protein kinase B serine 473 phosphorylation and glycogen synthesis. Both LXRα and LXRβ were expressed in human skeletal muscle and adipose tissue and there was no difference in their mRNA abundance in tissues from patients with type 2 diabetes compared with control subjects. In cultured muscle cells, LXR activation by T0901317 strongly increased expression of the genes encoding lipogenic enzymes, including sterol regulatory element binding protein 1c, fatty acid synthase and stearoyl-CoA desaturase 1, and also promoted triglyceride accumulation in the presence of a high glucose concentration. Importantly, these effects on lipid metabolism did not affect protein kinase B activation by insulin. Furthermore, LXR agonists did not modify insulin action in muscle cells from patients with type 2 diabetes. These data suggest that LXR agonists may lead to increased utilisation of lipids and glucose in muscle cells without affecting the mechanism of action of insulin. However, the long-term consequences of triglyceride accumulation in muscle should be evaluated before the development of effective LXR-based therapeutic agents.
         datePublished:2006-02-16T00:00:00Z
         dateModified:2006-02-16T00:00:00Z
         pageStart:990
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            Insulin action
            Lipogenesis
            Liver X receptor
            SREBP1c promoter
            Type 2 diabetes
            Internal Medicine
            Metabolic Diseases
            Human Physiology
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      headline:Activation of liver X receptors promotes lipid accumulation but does not alter insulin action in human skeletal muscle cells
      description:The aim of this study was to investigate the effects of liver X receptor (LXR) activation on lipid metabolism and insulin action in human skeletal muscle cells prepared from control subjects and from patients with type 2 diabetes. Cultured myotubes were obtained from muscle biopsies of 11 lean, healthy control subjects and ten patients with type 2 diabetes. The mRNA levels of LXR isoforms and lipogenic genes were estimated by RT-quantitative PCR, and the effects of LXR agonists on insulin action were evaluated by assays of protein kinase B serine 473 phosphorylation and glycogen synthesis. Both LXRα and LXRβ were expressed in human skeletal muscle and adipose tissue and there was no difference in their mRNA abundance in tissues from patients with type 2 diabetes compared with control subjects. In cultured muscle cells, LXR activation by T0901317 strongly increased expression of the genes encoding lipogenic enzymes, including sterol regulatory element binding protein 1c, fatty acid synthase and stearoyl-CoA desaturase 1, and also promoted triglyceride accumulation in the presence of a high glucose concentration. Importantly, these effects on lipid metabolism did not affect protein kinase B activation by insulin. Furthermore, LXR agonists did not modify insulin action in muscle cells from patients with type 2 diabetes. These data suggest that LXR agonists may lead to increased utilisation of lipids and glucose in muscle cells without affecting the mechanism of action of insulin. However, the long-term consequences of triglyceride accumulation in muscle should be evaluated before the development of effective LXR-based therapeutic agents.
      datePublished:2006-02-16T00:00:00Z
      dateModified:2006-02-16T00:00:00Z
      pageStart:990
      pageEnd:999
      sameAs:https://doi.org/10.1007/s00125-006-0140-8
      keywords:
         Human muscle cells
         Insulin action
         Lipogenesis
         Liver X receptor
         SREBP1c promoter
         Type 2 diabetes
         Internal Medicine
         Metabolic Diseases
         Human Physiology
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                     name:INSERM U449, INRA U1235, Laennec Faculty of Medicine, Claude Bernard University of Lyon, Lyon, France
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                     name:INSERM U449, INRA U1235, Laennec Faculty of Medicine, Claude Bernard University of Lyon, Lyon, France
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                  name:Claude Bernard University of Lyon
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                     name:INSERM U449, INRA U1235, Laennec Faculty of Medicine, Claude Bernard University of Lyon, Lyon, France
                     type:PostalAddress
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                     name:INSERM U449, INRA U1235, Laennec Faculty of Medicine, Claude Bernard University of Lyon, Lyon, France
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                     name:INSERM U449, INRA U1235, Laennec Faculty of Medicine, Claude Bernard University of Lyon, Lyon, France
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      name:E. Disse
      affiliation:
            name:Claude Bernard University of Lyon
            address:
               name:INSERM U449, INRA U1235, Laennec Faculty of Medicine, Claude Bernard University of Lyon, Lyon, France
               type:PostalAddress
            type:Organization
            name:Human Nutrition Research Center of Lyon
            address:
               name:Human Nutrition Research Center of Lyon, Lyon, France
               type:PostalAddress
            type:Organization
      name:J. Vouillarmet
      affiliation:
            name:Claude Bernard University of Lyon
            address:
               name:INSERM U449, INRA U1235, Laennec Faculty of Medicine, Claude Bernard University of Lyon, Lyon, France
               type:PostalAddress
            type:Organization
            name:Human Nutrition Research Center of Lyon
            address:
               name:Human Nutrition Research Center of Lyon, Lyon, France
               type:PostalAddress
            type:Organization
      name:R. Rabasa-Lhoret
      affiliation:
            name:Claude Bernard University of Lyon
            address:
               name:INSERM U449, INRA U1235, Laennec Faculty of Medicine, Claude Bernard University of Lyon, Lyon, France
               type:PostalAddress
            type:Organization
            name:Human Nutrition Research Center of Lyon
            address:
               name:Human Nutrition Research Center of Lyon, Lyon, France
               type:PostalAddress
            type:Organization
      name:M. Laville
      affiliation:
            name:Claude Bernard University of Lyon
            address:
               name:INSERM U449, INRA U1235, Laennec Faculty of Medicine, Claude Bernard University of Lyon, Lyon, France
               type:PostalAddress
            type:Organization
            name:Human Nutrition Research Center of Lyon
            address:
               name:Human Nutrition Research Center of Lyon, Lyon, France
               type:PostalAddress
            type:Organization
      name:D. Pruneau
      affiliation:
            name:Fournier-Pharma
            address:
               name:Department of Pharmacology, Fournier-Pharma, Daix, France
               type:PostalAddress
            type:Organization
      name:J. Rieusset
      affiliation:
            name:Claude Bernard University of Lyon
            address:
               name:INSERM U449, INRA U1235, Laennec Faculty of Medicine, Claude Bernard University of Lyon, Lyon, France
               type:PostalAddress
            type:Organization
      name:E. Lefai
      affiliation:
            name:Claude Bernard University of Lyon
            address:
               name:INSERM U449, INRA U1235, Laennec Faculty of Medicine, Claude Bernard University of Lyon, Lyon, France
               type:PostalAddress
            type:Organization
      name:H. Vidal
      affiliation:
            name:Claude Bernard University of Lyon
            address:
               name:INSERM U449, INRA U1235, Laennec Faculty of Medicine, Claude Bernard University of Lyon, Lyon, France
               type:PostalAddress
            type:Organization
            name:Faculté de Médecine R Laennec
            address:
               name:UMR INSERM U-449/INRA-1235, Faculté de Médecine R Laennec, Lyon, France
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:INSERM U449, INRA U1235, Laennec Faculty of Medicine, Claude Bernard University of Lyon, Lyon, France
      name:INSERM U449, INRA U1235, Laennec Faculty of Medicine, Claude Bernard University of Lyon, Lyon, France
      name:INSERM U449, INRA U1235, Laennec Faculty of Medicine, Claude Bernard University of Lyon, Lyon, France
      name:INSERM U449, INRA U1235, Laennec Faculty of Medicine, Claude Bernard University of Lyon, Lyon, France
      name:INSERM U449, INRA U1235, Laennec Faculty of Medicine, Claude Bernard University of Lyon, Lyon, France
      name:Human Nutrition Research Center of Lyon, Lyon, France
      name:INSERM U449, INRA U1235, Laennec Faculty of Medicine, Claude Bernard University of Lyon, Lyon, France
      name:Human Nutrition Research Center of Lyon, Lyon, France
      name:INSERM U449, INRA U1235, Laennec Faculty of Medicine, Claude Bernard University of Lyon, Lyon, France
      name:Human Nutrition Research Center of Lyon, Lyon, France
      name:INSERM U449, INRA U1235, Laennec Faculty of Medicine, Claude Bernard University of Lyon, Lyon, France
      name:Human Nutrition Research Center of Lyon, Lyon, France
      name:Department of Pharmacology, Fournier-Pharma, Daix, France
      name:INSERM U449, INRA U1235, Laennec Faculty of Medicine, Claude Bernard University of Lyon, Lyon, France
      name:INSERM U449, INRA U1235, Laennec Faculty of Medicine, Claude Bernard University of Lyon, Lyon, France
      name:INSERM U449, INRA U1235, Laennec Faculty of Medicine, Claude Bernard University of Lyon, Lyon, France
      name:UMR INSERM U-449/INRA-1235, Faculté de Médecine R Laennec, Lyon, France

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