We are analyzing https://link.springer.com/article/10.1007/s00125-009-1347-2.

Title:
Autophagy in human type 2 diabetes pancreatic beta cells | Diabetologia
Description:
Aims/hypothesis Beta cell loss contributes to type 2 diabetes, with increased apoptosis representing an underlying mechanism. Autophagy, i.e. the physiological degradation of damaged organelles and proteins, may, if altered, be associated with a distinct form of cell death. We studied several features of autophagy in beta cells from type 2 diabetic patients and assessed the role of metabolic perturbation and pharmacological intervention. Methods Pancreatic samples were obtained from organ donors and isolated islets prepared both by collagenase digestion and density gradient centrifugation. Beta cell morphology and morphometry were studied by electron microscopy. Gene expression studies were performed by quantitative RT-PCR. Results Using electron microscopy, we observed more dead beta cells in diabetic (2.24 ± 0.53%) than control (0.66 ± 0.52%) samples (p < 0.01). Massive vacuole overload (suggesting altered autophagy) was associated with 1.18 ± 0.54% dead beta cells in type 2 diabetic samples and with 0.36 ± 0.26% in control samples (p < 0.05). Density volume of autophagic vacuoles and autophagosomes was significantly higher in diabetic beta cells. Unchanged gene expression of beclin-1 and ATG1 (also known as ULK1), and reduced transcription of LAMP2 and cathepsin B and D was observed in type 2 diabetic islets. Exposure of non-diabetic islets to increased NEFA concentration led to a marked increase of vacuole accumulation, together with enhanced beta cell death, which was associated with decreased LAMP2 expression. Metformin ameliorated autophagy alterations in diabetic beta cells and beta cells exposed to NEFA, a process associated with normalisation of LAMP2 expression. Conclusions/interpretation Beta cells in human type 2 diabetes have signs of altered autophagy, which may contribute to loss of beta cell mass. To preserve beta cell mass in diabetic patients, it may be necessary to target multiple cell-death pathways.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

Science
Games
Health & Fitness

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 7,643,078 visitors per month in the current month.

check SE Ranking
check Ahrefs
check Similarweb
check Ubersuggest
check Semrush

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

We find it hard to spot revenue streams.

Some websites aren't about earning revenue; they're built to connect communities or raise awareness. There are numerous motivations behind creating websites. This might be one of them. Link.springer.com might be earning cash quietly, but we haven't detected the monetization method.

Keywords {🔍}

beta, cell, cells, autophagy, type, diabetic, diabetes, death, autophagic, article, islets, pancreatic, metformin, expression, vacuoles, lamp, cas, google, scholar, pubmed, altered, dead, vacuole, nefa, accumulation, control, fig, cathepsin, increased, samples, autophagosomes, atg, signs, human, apoptosis, organelles, gene, observed, exposure, mass, pisa, results, massive, beclin, nondiabetic, alterations, removal, membrane, privacy, cookies,

Topics {✒️}

diabetes-induced oxidative stress multiple cell-death pathways beta cell-specific deletion amp-activated protein kinase nefa-induced ceramide formation amp-regulated kinase family nefa-exposed beta cells ubiquinated-protein aggregates form pancreatic beta cells pancreatic beta-cells privacy choices/manage cookies beta cell mass human pancreatic islets messenger rna level gene expression studies beta cells exposed high-fat diet beta cell death beta-cell death autophagy-related gene dead beta cells beta cell morphology beta cell identity beta cell line beta cell dysfunction beta cell damage normal beta cell unchanged gene expression normal beta cells programmed cell death apoptotic cell death cell death modalities free fatty acids diabetic beta cells plasma membrane integrity autophagy-mediated death related subjects digesting mechanism responsible tumor suppressor mechanism major chromatin condensation reduced lamp2 expression quantitative rt-pcr defined cytoplasmic regions hydrolytic enzymes responsible local ethics committee close double membranes quantitative rt-pcr [2] realistic therapeutic target unique neuronal functions significantly lower expression

Questions {❓}

Meier JJ (2008) Beta cell mass in diabetes: a realistic therapeutic target?

Schema {🗺️}

WebPage:
      mainEntity:
         headline:Autophagy in human type 2 diabetes pancreatic beta cells
         description:Beta cell loss contributes to type 2 diabetes, with increased apoptosis representing an underlying mechanism. Autophagy, i.e. the physiological degradation of damaged organelles and proteins, may, if altered, be associated with a distinct form of cell death. We studied several features of autophagy in beta cells from type 2 diabetic patients and assessed the role of metabolic perturbation and pharmacological intervention. Pancreatic samples were obtained from organ donors and isolated islets prepared both by collagenase digestion and density gradient centrifugation. Beta cell morphology and morphometry were studied by electron microscopy. Gene expression studies were performed by quantitative RT-PCR. Using electron microscopy, we observed more dead beta cells in diabetic (2.24 ± 0.53%) than control (0.66 ± 0.52%) samples (p < 0.01). Massive vacuole overload (suggesting altered autophagy) was associated with 1.18 ± 0.54% dead beta cells in type 2 diabetic samples and with 0.36 ± 0.26% in control samples (p < 0.05). Density volume of autophagic vacuoles and autophagosomes was significantly higher in diabetic beta cells. Unchanged gene expression of beclin-1 and ATG1 (also known as ULK1), and reduced transcription of LAMP2 and cathepsin B and D was observed in type 2 diabetic islets. Exposure of non-diabetic islets to increased NEFA concentration led to a marked increase of vacuole accumulation, together with enhanced beta cell death, which was associated with decreased LAMP2 expression. Metformin ameliorated autophagy alterations in diabetic beta cells and beta cells exposed to NEFA, a process associated with normalisation of LAMP2 expression. Beta cells in human type 2 diabetes have signs of altered autophagy, which may contribute to loss of beta cell mass. To preserve beta cell mass in diabetic patients, it may be necessary to target multiple cell-death pathways.
         datePublished:2009-04-15T00:00:00Z
         dateModified:2009-04-15T00:00:00Z
         pageStart:1083
         pageEnd:1086
         sameAs:https://doi.org/10.1007/s00125-009-1347-2
         keywords:
            Autophagy
            Metformin
            NEFA
            Pancreatic beta cells
            Internal Medicine
            Metabolic Diseases
            Human Physiology
         image:
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs00125-009-1347-2/MediaObjects/125_2009_1347_Fig1_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs00125-009-1347-2/MediaObjects/125_2009_1347_Fig2_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs00125-009-1347-2/MediaObjects/125_2009_1347_Fig3_HTML.gif
         isPartOf:
            name:Diabetologia
            issn:
               1432-0428
               0012-186X
            volumeNumber:52
            type:
               Periodical
               PublicationVolume
         publisher:
            name:Springer-Verlag
            logo:
               url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
               type:ImageObject
            type:Organization
         author:
               name:M. Masini
               affiliation:
                     name:University of Pisa
                     address:
                        name:Department of Experimental Pathology, University of Pisa, Pisa, Italy
                        type:PostalAddress
                     type:Organization
               type:Person
               name:M. Bugliani
               affiliation:
                     name:Department of Endocrinology and Metabolism
                     address:
                        name:Department of Endocrinology and Metabolism, Pisa, Italy
                        type:PostalAddress
                     type:Organization
               type:Person
               name:R. Lupi
               affiliation:
                     name:Department of Endocrinology and Metabolism
                     address:
                        name:Department of Endocrinology and Metabolism, Pisa, Italy
                        type:PostalAddress
                     type:Organization
               type:Person
               name:S. del Guerra
               affiliation:
                     name:Department of Endocrinology and Metabolism
                     address:
                        name:Department of Endocrinology and Metabolism, Pisa, Italy
                        type:PostalAddress
                     type:Organization
               type:Person
               name:U. Boggi
               affiliation:
                     name:University of Pisa
                     address:
                        name:Department of Oncology, Transplants and Advanced Technologies in Medicine, University of Pisa, Pisa, Italy
                        type:PostalAddress
                     type:Organization
               type:Person
               name:F. Filipponi
               affiliation:
                     name:University of Pisa
                     address:
                        name:Department of Liver Transplant, University of Pisa, Pisa, Italy
                        type:PostalAddress
                     type:Organization
               type:Person
               name:L. Marselli
               affiliation:
                     name:Department of Endocrinology and Metabolism
                     address:
                        name:Department of Endocrinology and Metabolism, Pisa, Italy
                        type:PostalAddress
                     type:Organization
               type:Person
               name:P. Masiello
               affiliation:
                     name:University of Pisa
                     address:
                        name:Department of Experimental Pathology, University of Pisa, Pisa, Italy
                        type:PostalAddress
                     type:Organization
               type:Person
               name:P. Marchetti
               affiliation:
                     name:Department of Endocrinology and Metabolism
                     address:
                        name:Department of Endocrinology and Metabolism, Pisa, Italy
                        type:PostalAddress
                     type:Organization
               email:[email protected]
               type:Person
         isAccessibleForFree:1
         type:ScholarlyArticle
      context:https://schema.org
ScholarlyArticle:
      headline:Autophagy in human type 2 diabetes pancreatic beta cells
      description:Beta cell loss contributes to type 2 diabetes, with increased apoptosis representing an underlying mechanism. Autophagy, i.e. the physiological degradation of damaged organelles and proteins, may, if altered, be associated with a distinct form of cell death. We studied several features of autophagy in beta cells from type 2 diabetic patients and assessed the role of metabolic perturbation and pharmacological intervention. Pancreatic samples were obtained from organ donors and isolated islets prepared both by collagenase digestion and density gradient centrifugation. Beta cell morphology and morphometry were studied by electron microscopy. Gene expression studies were performed by quantitative RT-PCR. Using electron microscopy, we observed more dead beta cells in diabetic (2.24 ± 0.53%) than control (0.66 ± 0.52%) samples (p < 0.01). Massive vacuole overload (suggesting altered autophagy) was associated with 1.18 ± 0.54% dead beta cells in type 2 diabetic samples and with 0.36 ± 0.26% in control samples (p < 0.05). Density volume of autophagic vacuoles and autophagosomes was significantly higher in diabetic beta cells. Unchanged gene expression of beclin-1 and ATG1 (also known as ULK1), and reduced transcription of LAMP2 and cathepsin B and D was observed in type 2 diabetic islets. Exposure of non-diabetic islets to increased NEFA concentration led to a marked increase of vacuole accumulation, together with enhanced beta cell death, which was associated with decreased LAMP2 expression. Metformin ameliorated autophagy alterations in diabetic beta cells and beta cells exposed to NEFA, a process associated with normalisation of LAMP2 expression. Beta cells in human type 2 diabetes have signs of altered autophagy, which may contribute to loss of beta cell mass. To preserve beta cell mass in diabetic patients, it may be necessary to target multiple cell-death pathways.
      datePublished:2009-04-15T00:00:00Z
      dateModified:2009-04-15T00:00:00Z
      pageStart:1083
      pageEnd:1086
      sameAs:https://doi.org/10.1007/s00125-009-1347-2
      keywords:
         Autophagy
         Metformin
         NEFA
         Pancreatic beta cells
         Internal Medicine
         Metabolic Diseases
         Human Physiology
      image:
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs00125-009-1347-2/MediaObjects/125_2009_1347_Fig1_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs00125-009-1347-2/MediaObjects/125_2009_1347_Fig2_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs00125-009-1347-2/MediaObjects/125_2009_1347_Fig3_HTML.gif
      isPartOf:
         name:Diabetologia
         issn:
            1432-0428
            0012-186X
         volumeNumber:52
         type:
            Periodical
            PublicationVolume
      publisher:
         name:Springer-Verlag
         logo:
            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
         type:Organization
      author:
            name:M. Masini
            affiliation:
                  name:University of Pisa
                  address:
                     name:Department of Experimental Pathology, University of Pisa, Pisa, Italy
                     type:PostalAddress
                  type:Organization
            type:Person
            name:M. Bugliani
            affiliation:
                  name:Department of Endocrinology and Metabolism
                  address:
                     name:Department of Endocrinology and Metabolism, Pisa, Italy
                     type:PostalAddress
                  type:Organization
            type:Person
            name:R. Lupi
            affiliation:
                  name:Department of Endocrinology and Metabolism
                  address:
                     name:Department of Endocrinology and Metabolism, Pisa, Italy
                     type:PostalAddress
                  type:Organization
            type:Person
            name:S. del Guerra
            affiliation:
                  name:Department of Endocrinology and Metabolism
                  address:
                     name:Department of Endocrinology and Metabolism, Pisa, Italy
                     type:PostalAddress
                  type:Organization
            type:Person
            name:U. Boggi
            affiliation:
                  name:University of Pisa
                  address:
                     name:Department of Oncology, Transplants and Advanced Technologies in Medicine, University of Pisa, Pisa, Italy
                     type:PostalAddress
                  type:Organization
            type:Person
            name:F. Filipponi
            affiliation:
                  name:University of Pisa
                  address:
                     name:Department of Liver Transplant, University of Pisa, Pisa, Italy
                     type:PostalAddress
                  type:Organization
            type:Person
            name:L. Marselli
            affiliation:
                  name:Department of Endocrinology and Metabolism
                  address:
                     name:Department of Endocrinology and Metabolism, Pisa, Italy
                     type:PostalAddress
                  type:Organization
            type:Person
            name:P. Masiello
            affiliation:
                  name:University of Pisa
                  address:
                     name:Department of Experimental Pathology, University of Pisa, Pisa, Italy
                     type:PostalAddress
                  type:Organization
            type:Person
            name:P. Marchetti
            affiliation:
                  name:Department of Endocrinology and Metabolism
                  address:
                     name:Department of Endocrinology and Metabolism, Pisa, Italy
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
      isAccessibleForFree:1
["Periodical","PublicationVolume"]:
      name:Diabetologia
      issn:
         1432-0428
         0012-186X
      volumeNumber:52
Organization:
      name:Springer-Verlag
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:University of Pisa
      address:
         name:Department of Experimental Pathology, University of Pisa, Pisa, Italy
         type:PostalAddress
      name:Department of Endocrinology and Metabolism
      address:
         name:Department of Endocrinology and Metabolism, Pisa, Italy
         type:PostalAddress
      name:Department of Endocrinology and Metabolism
      address:
         name:Department of Endocrinology and Metabolism, Pisa, Italy
         type:PostalAddress
      name:Department of Endocrinology and Metabolism
      address:
         name:Department of Endocrinology and Metabolism, Pisa, Italy
         type:PostalAddress
      name:University of Pisa
      address:
         name:Department of Oncology, Transplants and Advanced Technologies in Medicine, University of Pisa, Pisa, Italy
         type:PostalAddress
      name:University of Pisa
      address:
         name:Department of Liver Transplant, University of Pisa, Pisa, Italy
         type:PostalAddress
      name:Department of Endocrinology and Metabolism
      address:
         name:Department of Endocrinology and Metabolism, Pisa, Italy
         type:PostalAddress
      name:University of Pisa
      address:
         name:Department of Experimental Pathology, University of Pisa, Pisa, Italy
         type:PostalAddress
      name:Department of Endocrinology and Metabolism
      address:
         name:Department of Endocrinology and Metabolism, Pisa, Italy
         type:PostalAddress
ImageObject:
      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:M. Masini
      affiliation:
            name:University of Pisa
            address:
               name:Department of Experimental Pathology, University of Pisa, Pisa, Italy
               type:PostalAddress
            type:Organization
      name:M. Bugliani
      affiliation:
            name:Department of Endocrinology and Metabolism
            address:
               name:Department of Endocrinology and Metabolism, Pisa, Italy
               type:PostalAddress
            type:Organization
      name:R. Lupi
      affiliation:
            name:Department of Endocrinology and Metabolism
            address:
               name:Department of Endocrinology and Metabolism, Pisa, Italy
               type:PostalAddress
            type:Organization
      name:S. del Guerra
      affiliation:
            name:Department of Endocrinology and Metabolism
            address:
               name:Department of Endocrinology and Metabolism, Pisa, Italy
               type:PostalAddress
            type:Organization
      name:U. Boggi
      affiliation:
            name:University of Pisa
            address:
               name:Department of Oncology, Transplants and Advanced Technologies in Medicine, University of Pisa, Pisa, Italy
               type:PostalAddress
            type:Organization
      name:F. Filipponi
      affiliation:
            name:University of Pisa
            address:
               name:Department of Liver Transplant, University of Pisa, Pisa, Italy
               type:PostalAddress
            type:Organization
      name:L. Marselli
      affiliation:
            name:Department of Endocrinology and Metabolism
            address:
               name:Department of Endocrinology and Metabolism, Pisa, Italy
               type:PostalAddress
            type:Organization
      name:P. Masiello
      affiliation:
            name:University of Pisa
            address:
               name:Department of Experimental Pathology, University of Pisa, Pisa, Italy
               type:PostalAddress
            type:Organization
      name:P. Marchetti
      affiliation:
            name:Department of Endocrinology and Metabolism
            address:
               name:Department of Endocrinology and Metabolism, Pisa, Italy
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Department of Experimental Pathology, University of Pisa, Pisa, Italy
      name:Department of Endocrinology and Metabolism, Pisa, Italy
      name:Department of Endocrinology and Metabolism, Pisa, Italy
      name:Department of Endocrinology and Metabolism, Pisa, Italy
      name:Department of Oncology, Transplants and Advanced Technologies in Medicine, University of Pisa, Pisa, Italy
      name:Department of Liver Transplant, University of Pisa, Pisa, Italy
      name:Department of Endocrinology and Metabolism, Pisa, Italy
      name:Department of Experimental Pathology, University of Pisa, Pisa, Italy
      name:Department of Endocrinology and Metabolism, Pisa, Italy

External Links {🔗}(80)

Analytics and Tracking {📊}

Google Tag Manager

Libraries {📚}

Clipboard.js
Prism.js

CDN Services {📦}

Crossref

3.93s.

LINK . SPRINGER . COM {}