We are analyzing https://link.springer.com/article/10.1007/s11010-010-0520-8.

Title:
Activation of PPARδ promotes mitochondrial energy metabolism and decreases basal insulin secretion in palmitate-treated β-cells | Molecular and Cellular Biochemistry
Description:
The peroxisome proliferator-activated receptor δ (PPARδ) regulates the expression of genes involved in cellular lipid and cell energy metabolism in many metabolically active tissues, such as liver, muscle, and fat, and plays a role in the cellular response to stress and environmental stimuli. The particular role of PPARδ in insulin-secreting β-cells, however, is not well understood; we recently identified the cell-specific role of PPARδ on mitochondrial energy metabolism and insulin secretion in lipotoxic β-cells. After treatment of HIT-T15 cells, a syrian hamster pancreatic β-cell line, with high concentrations of palmitate and/or the specific PPARδ agonist GW501516, we detected the gene expression changes for transcripts, such as peroxisome proliferator-activated receptor gamma co-activator 1 (PGC-1α), nuclear respiratory factor 1 (NRF-1), mitochondrial transcription factor A (mtTFA), the protein levels of the mitochondria uncoupling protein 2 (UCP2), mitochondrial morphology, the insulin secretion capacity and ATP/ADP ratio. Our results show that GW501516 treatment promoted generation of mitochondrial ATP, as well as expression levels of PGC-1α, NRF-1 and mtTFA, decreased basal insulin secretion, but had no effect on glucose-stimulated insulin secretion (GSIS), increased amounts of UCP2 and changed ATP-to-ADP ratio, improved mitochondrial morphology in palmitate-treated β-cells. GW501516-induced activation of PPARδ enhanced mitochondrial energy metabolism, but also promoted a concomitant mitochondrial uncoupling and resulted in decreased basal insulin secretion and restricted GSIS; this observation indicated the possible action of a protective mechanism responding to the alleviation of excessive lipid load and basal insulin secretion in lipotoxic β-cells.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

Health & Fitness
Science
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.
However, some sources were not loaded, we suggest to reload the page to get complete results.

check SE Ranking
check Ahrefs
check Similarweb
check Ubersuggest
check Semrush

How Does Link.springer.com Make Money? {💸}

We can't figure out the monetization strategy.

Not all websites focus on profit; some are designed to educate, connect people, or share useful tools. People create websites for numerous reasons. And this could be one such example. Link.springer.com could have a money-making trick up its sleeve, but it's undetectable for now.

Keywords {🔍}

article, google, scholar, pubmed, cas, insulin, mitochondrial, secretion, pparδ, metabolism, peroxisome, proliferatoractivated, activation, diabetes, energy, receptor, muscle, expression, role, cells, usa, content, βcells, cell, proc, natl, acad, sci, privacy, cookies, basal, pancreatic, gene, coactivator, pgcα, transcription, protein, uncoupling, fatty, publish, search, cellular, promotes, june, βcell, factor, glucosestimulated, access, metabolic, acid,

Topics {✒️}

qing-guo lü & nan-wei tong peroxisome proliferator-activated receptor 6-dimethoxyisoflavone-7-o-β-d-glucopyranoside peroxisome proliferator-activated receptors palmitate-treated β-cells published month download article/chapter glucose-stimulated insulin secretion nan-wei tong insulin-secreting β-cells fatty acid excess palmitate-treated β-cells diabetic db/db mice katp channel-dependent pathway mitochondrial energy metabolism slow-twitch muscle fibres cell energy metabolism basal insulin secretion activator pgc-1α drives δ promotes reversal anaerobic glucose metabolism insulin secretion capacity attenuates metabolic syndrome multiple metabolic abnormalities full article pdf pancreatic β-cell high-fat diet pancreatic β cells βhc9 cells deficient ppar{delta} pancreatic beta cells privacy choices/manage cookies mitochondrial dna transcription β-cell model lipotoxic β-cells improves insulin sensitivity improved insulin sensitivity energy metabolism glucose-dependent esterification mitochondrial transcription factor concomitant mitochondrial uncoupling abnormal weight control thermogenic coactivator pgc gw501516-induced activation related subjects mitochondrial gene expression glucose metabolism insulin secretion state key laboratory xiao-yü li hit-t15 cells

Questions {❓}

Lameloise N, Muzzin P, Prentki M et al (2001) Uncoupling protein 2: a possible link between fatty acid excess and impaired glucose-induced insulin secretion?

Schema {🗺️}

WebPage:
      mainEntity:
         headline:Activation of PPARδ promotes mitochondrial energy metabolism and decreases basal insulin secretion in palmitate-treated β-cells
         description:The peroxisome proliferator-activated receptor δ (PPARδ) regulates the expression of genes involved in cellular lipid and cell energy metabolism in many metabolically active tissues, such as liver, muscle, and fat, and plays a role in the cellular response to stress and environmental stimuli. The particular role of PPARδ in insulin-secreting β-cells, however, is not well understood; we recently identified the cell-specific role of PPARδ on mitochondrial energy metabolism and insulin secretion in lipotoxic β-cells. After treatment of HIT-T15 cells, a syrian hamster pancreatic β-cell line, with high concentrations of palmitate and/or the specific PPARδ agonist GW501516, we detected the gene expression changes for transcripts, such as peroxisome proliferator-activated receptor gamma co-activator 1 (PGC-1α), nuclear respiratory factor 1 (NRF-1), mitochondrial transcription factor A (mtTFA), the protein levels of the mitochondria uncoupling protein 2 (UCP2), mitochondrial morphology, the insulin secretion capacity and ATP/ADP ratio. Our results show that GW501516 treatment promoted generation of mitochondrial ATP, as well as expression levels of PGC-1α, NRF-1 and mtTFA, decreased basal insulin secretion, but had no effect on glucose-stimulated insulin secretion (GSIS), increased amounts of UCP2 and changed ATP-to-ADP ratio, improved mitochondrial morphology in palmitate-treated β-cells. GW501516-induced activation of PPARδ enhanced mitochondrial energy metabolism, but also promoted a concomitant mitochondrial uncoupling and resulted in decreased basal insulin secretion and restricted GSIS; this observation indicated the possible action of a protective mechanism responding to the alleviation of excessive lipid load and basal insulin secretion in lipotoxic β-cells.
         datePublished:2010-06-24T00:00:00Z
         dateModified:2010-06-24T00:00:00Z
         pageStart:249
         pageEnd:256
         sameAs:https://doi.org/10.1007/s11010-010-0520-8
         keywords:
            PPARδ
            β-cell
            Mitochondria
            Insulin secretion
            Energy metabolism
            Biochemistry
            general
            Cardiology
            Cancer Research
            Medical Biochemistry
         image:
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs11010-010-0520-8/MediaObjects/11010_2010_520_Fig1_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs11010-010-0520-8/MediaObjects/11010_2010_520_Fig2_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs11010-010-0520-8/MediaObjects/11010_2010_520_Fig3_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs11010-010-0520-8/MediaObjects/11010_2010_520_Fig4_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs11010-010-0520-8/MediaObjects/11010_2010_520_Fig5_HTML.jpg
         isPartOf:
            name:Molecular and Cellular Biochemistry
            issn:
               1573-4919
               0300-8177
            volumeNumber:343
            type:
               Periodical
               PublicationVolume
         publisher:
            name:Springer US
            logo:
               url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
               type:ImageObject
            type:Organization
         author:
               name:Li Jiang
               affiliation:
                     name:West China Hospital, Sichuan University
                     address:
                        name:Department of Endocrinology, West China Hospital, Sichuan University, Chengdu, China
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Jun Wan
               affiliation:
                     name:West China Hospital, Sichuan University
                     address:
                        name:Department of Endocrinology, West China Hospital, Sichuan University, Chengdu, China
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Lin-qiu Ke
               affiliation:
                     name:West China Hospital, Sichuan University
                     address:
                        name:Department of Endocrinology, West China Hospital, Sichuan University, Chengdu, China
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Qing-guo Lü
               affiliation:
                     name:West China Hospital, Sichuan University
                     address:
                        name:Department of Endocrinology, West China Hospital, Sichuan University, Chengdu, China
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Nan-wei Tong
               affiliation:
                     name:West China Hospital, Sichuan University
                     address:
                        name:Department of Endocrinology, West China Hospital, Sichuan University, Chengdu, China
                        type:PostalAddress
                     type:Organization
               email:[email protected]
               type:Person
         isAccessibleForFree:
         hasPart:
            isAccessibleForFree:
            cssSelector:.main-content
            type:WebPageElement
         type:ScholarlyArticle
      context:https://schema.org
ScholarlyArticle:
      headline:Activation of PPARδ promotes mitochondrial energy metabolism and decreases basal insulin secretion in palmitate-treated β-cells
      description:The peroxisome proliferator-activated receptor δ (PPARδ) regulates the expression of genes involved in cellular lipid and cell energy metabolism in many metabolically active tissues, such as liver, muscle, and fat, and plays a role in the cellular response to stress and environmental stimuli. The particular role of PPARδ in insulin-secreting β-cells, however, is not well understood; we recently identified the cell-specific role of PPARδ on mitochondrial energy metabolism and insulin secretion in lipotoxic β-cells. After treatment of HIT-T15 cells, a syrian hamster pancreatic β-cell line, with high concentrations of palmitate and/or the specific PPARδ agonist GW501516, we detected the gene expression changes for transcripts, such as peroxisome proliferator-activated receptor gamma co-activator 1 (PGC-1α), nuclear respiratory factor 1 (NRF-1), mitochondrial transcription factor A (mtTFA), the protein levels of the mitochondria uncoupling protein 2 (UCP2), mitochondrial morphology, the insulin secretion capacity and ATP/ADP ratio. Our results show that GW501516 treatment promoted generation of mitochondrial ATP, as well as expression levels of PGC-1α, NRF-1 and mtTFA, decreased basal insulin secretion, but had no effect on glucose-stimulated insulin secretion (GSIS), increased amounts of UCP2 and changed ATP-to-ADP ratio, improved mitochondrial morphology in palmitate-treated β-cells. GW501516-induced activation of PPARδ enhanced mitochondrial energy metabolism, but also promoted a concomitant mitochondrial uncoupling and resulted in decreased basal insulin secretion and restricted GSIS; this observation indicated the possible action of a protective mechanism responding to the alleviation of excessive lipid load and basal insulin secretion in lipotoxic β-cells.
      datePublished:2010-06-24T00:00:00Z
      dateModified:2010-06-24T00:00:00Z
      pageStart:249
      pageEnd:256
      sameAs:https://doi.org/10.1007/s11010-010-0520-8
      keywords:
         PPARδ
         β-cell
         Mitochondria
         Insulin secretion
         Energy metabolism
         Biochemistry
         general
         Cardiology
         Cancer Research
         Medical Biochemistry
      image:
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs11010-010-0520-8/MediaObjects/11010_2010_520_Fig1_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs11010-010-0520-8/MediaObjects/11010_2010_520_Fig2_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs11010-010-0520-8/MediaObjects/11010_2010_520_Fig3_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs11010-010-0520-8/MediaObjects/11010_2010_520_Fig4_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs11010-010-0520-8/MediaObjects/11010_2010_520_Fig5_HTML.jpg
      isPartOf:
         name:Molecular and Cellular Biochemistry
         issn:
            1573-4919
            0300-8177
         volumeNumber:343
         type:
            Periodical
            PublicationVolume
      publisher:
         name:Springer US
         logo:
            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
         type:Organization
      author:
            name:Li Jiang
            affiliation:
                  name:West China Hospital, Sichuan University
                  address:
                     name:Department of Endocrinology, West China Hospital, Sichuan University, Chengdu, China
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Jun Wan
            affiliation:
                  name:West China Hospital, Sichuan University
                  address:
                     name:Department of Endocrinology, West China Hospital, Sichuan University, Chengdu, China
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Lin-qiu Ke
            affiliation:
                  name:West China Hospital, Sichuan University
                  address:
                     name:Department of Endocrinology, West China Hospital, Sichuan University, Chengdu, China
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Qing-guo Lü
            affiliation:
                  name:West China Hospital, Sichuan University
                  address:
                     name:Department of Endocrinology, West China Hospital, Sichuan University, Chengdu, China
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Nan-wei Tong
            affiliation:
                  name:West China Hospital, Sichuan University
                  address:
                     name:Department of Endocrinology, West China Hospital, Sichuan University, Chengdu, China
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
      isAccessibleForFree:
      hasPart:
         isAccessibleForFree:
         cssSelector:.main-content
         type:WebPageElement
["Periodical","PublicationVolume"]:
      name:Molecular and Cellular Biochemistry
      issn:
         1573-4919
         0300-8177
      volumeNumber:343
Organization:
      name:Springer US
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:West China Hospital, Sichuan University
      address:
         name:Department of Endocrinology, West China Hospital, Sichuan University, Chengdu, China
         type:PostalAddress
      name:West China Hospital, Sichuan University
      address:
         name:Department of Endocrinology, West China Hospital, Sichuan University, Chengdu, China
         type:PostalAddress
      name:West China Hospital, Sichuan University
      address:
         name:Department of Endocrinology, West China Hospital, Sichuan University, Chengdu, China
         type:PostalAddress
      name:West China Hospital, Sichuan University
      address:
         name:Department of Endocrinology, West China Hospital, Sichuan University, Chengdu, China
         type:PostalAddress
      name:West China Hospital, Sichuan University
      address:
         name:Department of Endocrinology, West China Hospital, Sichuan University, Chengdu, China
         type:PostalAddress
ImageObject:
      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:Li Jiang
      affiliation:
            name:West China Hospital, Sichuan University
            address:
               name:Department of Endocrinology, West China Hospital, Sichuan University, Chengdu, China
               type:PostalAddress
            type:Organization
      name:Jun Wan
      affiliation:
            name:West China Hospital, Sichuan University
            address:
               name:Department of Endocrinology, West China Hospital, Sichuan University, Chengdu, China
               type:PostalAddress
            type:Organization
      name:Lin-qiu Ke
      affiliation:
            name:West China Hospital, Sichuan University
            address:
               name:Department of Endocrinology, West China Hospital, Sichuan University, Chengdu, China
               type:PostalAddress
            type:Organization
      name:Qing-guo Lü
      affiliation:
            name:West China Hospital, Sichuan University
            address:
               name:Department of Endocrinology, West China Hospital, Sichuan University, Chengdu, China
               type:PostalAddress
            type:Organization
      name:Nan-wei Tong
      affiliation:
            name:West China Hospital, Sichuan University
            address:
               name:Department of Endocrinology, West China Hospital, Sichuan University, Chengdu, China
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Department of Endocrinology, West China Hospital, Sichuan University, Chengdu, China
      name:Department of Endocrinology, West China Hospital, Sichuan University, Chengdu, China
      name:Department of Endocrinology, West China Hospital, Sichuan University, Chengdu, China
      name:Department of Endocrinology, West China Hospital, Sichuan University, Chengdu, China
      name:Department of Endocrinology, West China Hospital, Sichuan University, Chengdu, China
WebPageElement:
      isAccessibleForFree:
      cssSelector:.main-content

External Links {🔗}(127)

Analytics and Tracking {📊}

Google Tag Manager

Libraries {📚}

Clipboard.js
Prism.js

CDN Services {📦}

Crossref

4.22s.

LINK . SPRINGER . COM {}