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Are we overestimating the loss of beta cells in type 2 diabetes?
Aims/hypothesis Previous work has demonstrated that beta cell amount (whether measured as beta cell mass, beta cell volume or insulin-positive area) is decreased in type 2 diabetes; however, recent findings suggest that mechanisms other than death may contribute to beta cell failure in this disease....
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| Published in: | Diabetologia 2014-02, Vol.57 (2), p.362-365 |
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| container_title | Diabetologia |
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| creator | Marselli, Lorella Suleiman, Mara Masini, Matilde Campani, Daniela Bugliani, Marco Syed, Farooq Martino, Luisa Focosi, Daniele Scatena, Fabrizio Olimpico, Francesco Filipponi, Franco Masiello, Pellegrino Boggi, Ugo Marchetti, Piero |
| description | Aims/hypothesis
Previous work has demonstrated that beta cell amount (whether measured as beta cell mass, beta cell volume or insulin-positive area) is decreased in type 2 diabetes; however, recent findings suggest that mechanisms other than death may contribute to beta cell failure in this disease. To better characterise beta cell mass and function in type 2 diabetes, we performed morphological, ultra-structural and functional studies using histological samples and isolated islets.
Methods
Pancreases from ten non-diabetic (ND) and ten matched type 2 diabetic organ donors were studied by insulin, glucagon and chromogranin A immunocytochemistry and electron microscopy (EM). Glucose-stimulated insulin secretion was assessed using isolated islets and studies were performed using independent ND islet preparations after 24 h exposure to 22.2 mmol/l glucose.
Results
Immunocytochemistry showed that the fractional islet insulin-positive area was lower in type 2 diabetic islets (54.9 ± 6.3% vs 72.1 ± 8.7%,
p
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| doi_str_mv | 10.1007/s00125-013-3098-3 |
| format | article |
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Previous work has demonstrated that beta cell amount (whether measured as beta cell mass, beta cell volume or insulin-positive area) is decreased in type 2 diabetes; however, recent findings suggest that mechanisms other than death may contribute to beta cell failure in this disease. To better characterise beta cell mass and function in type 2 diabetes, we performed morphological, ultra-structural and functional studies using histological samples and isolated islets.
Methods
Pancreases from ten non-diabetic (ND) and ten matched type 2 diabetic organ donors were studied by insulin, glucagon and chromogranin A immunocytochemistry and electron microscopy (EM). Glucose-stimulated insulin secretion was assessed using isolated islets and studies were performed using independent ND islet preparations after 24 h exposure to 22.2 mmol/l glucose.
Results
Immunocytochemistry showed that the fractional islet insulin-positive area was lower in type 2 diabetic islets (54.9 ± 6.3% vs 72.1 ± 8.7%,
p
< 0.01), whereas glucagon (23.3 ± 5.4% vs 20.2 ± 5.3%) and chromogranin A (86.4 ± 6.1% vs 89.0 ± 5.5%) staining was similar between the two groups. EM showed that the proportion of beta cells in type 2 diabetic islets was only marginally decreased; marked beta cell degranulation was found in diabetic beta cells; these findings were all reproduced after exposing isolated ND islets to high glucose. Glucose-stimulated insulin secretion was 40–50% lower from type 2 diabetic islets (
p
< 0.01), which again was mimicked by culturing non-diabetic islets in high glucose.
Conclusions/interpretation
These results suggest that, at least in subgroups of type 2 diabetic patients, the loss of beta cells as assessed so far might be overestimated, possibly due to changes in beta cell phenotype other than death, also contributing to beta cell failure in type 2 diabetes.</description><identifier>ISSN: 0012-186X</identifier><identifier>EISSN: 1432-0428</identifier><identifier>DOI: 10.1007/s00125-013-3098-3</identifier><identifier>PMID: 24233056</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Aged ; Antibodies ; Biological and medical sciences ; Chromogranin A - metabolism ; Diabetes ; Diabetes Mellitus, Type 2 - metabolism ; Diabetes Mellitus, Type 2 - pathology ; Diabetes. Impaired glucose tolerance ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Etiopathogenesis. Screening. Investigations. Target tissue resistance ; Female ; Gastrointestinal surgery ; Glucagon ; Glucagon - metabolism ; Glucose ; Human Physiology ; Humans ; Immunohistochemistry ; Insulin ; Insulin - metabolism ; Insulin-Secreting Cells - pathology ; Internal Medicine ; Male ; Medical sciences ; Medicine ; Medicine & Public Health ; Metabolic Diseases ; Microscopy ; Microscopy, Electron ; Morphology ; Pancreas - pathology ; Short Communication</subject><ispartof>Diabetologia, 2014-02, Vol.57 (2), p.362-365</ispartof><rights>Springer-Verlag Berlin Heidelberg 2013</rights><rights>2015 INIST-CNRS</rights><rights>Springer-Verlag Berlin Heidelberg 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c445t-ab5976148d6337deada380c09029fd0c6215807a58796c031e3cf1dd42b43ebd3</citedby><cites>FETCH-LOGICAL-c445t-ab5976148d6337deada380c09029fd0c6215807a58796c031e3cf1dd42b43ebd3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=28541529$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24233056$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Marselli, Lorella</creatorcontrib><creatorcontrib>Suleiman, Mara</creatorcontrib><creatorcontrib>Masini, Matilde</creatorcontrib><creatorcontrib>Campani, Daniela</creatorcontrib><creatorcontrib>Bugliani, Marco</creatorcontrib><creatorcontrib>Syed, Farooq</creatorcontrib><creatorcontrib>Martino, Luisa</creatorcontrib><creatorcontrib>Focosi, Daniele</creatorcontrib><creatorcontrib>Scatena, Fabrizio</creatorcontrib><creatorcontrib>Olimpico, Francesco</creatorcontrib><creatorcontrib>Filipponi, Franco</creatorcontrib><creatorcontrib>Masiello, Pellegrino</creatorcontrib><creatorcontrib>Boggi, Ugo</creatorcontrib><creatorcontrib>Marchetti, Piero</creatorcontrib><title>Are we overestimating the loss of beta cells in type 2 diabetes?</title><title>Diabetologia</title><addtitle>Diabetologia</addtitle><addtitle>Diabetologia</addtitle><description>Aims/hypothesis
Previous work has demonstrated that beta cell amount (whether measured as beta cell mass, beta cell volume or insulin-positive area) is decreased in type 2 diabetes; however, recent findings suggest that mechanisms other than death may contribute to beta cell failure in this disease. To better characterise beta cell mass and function in type 2 diabetes, we performed morphological, ultra-structural and functional studies using histological samples and isolated islets.
Methods
Pancreases from ten non-diabetic (ND) and ten matched type 2 diabetic organ donors were studied by insulin, glucagon and chromogranin A immunocytochemistry and electron microscopy (EM). Glucose-stimulated insulin secretion was assessed using isolated islets and studies were performed using independent ND islet preparations after 24 h exposure to 22.2 mmol/l glucose.
Results
Immunocytochemistry showed that the fractional islet insulin-positive area was lower in type 2 diabetic islets (54.9 ± 6.3% vs 72.1 ± 8.7%,
p
< 0.01), whereas glucagon (23.3 ± 5.4% vs 20.2 ± 5.3%) and chromogranin A (86.4 ± 6.1% vs 89.0 ± 5.5%) staining was similar between the two groups. EM showed that the proportion of beta cells in type 2 diabetic islets was only marginally decreased; marked beta cell degranulation was found in diabetic beta cells; these findings were all reproduced after exposing isolated ND islets to high glucose. Glucose-stimulated insulin secretion was 40–50% lower from type 2 diabetic islets (
p
< 0.01), which again was mimicked by culturing non-diabetic islets in high glucose.
Conclusions/interpretation
These results suggest that, at least in subgroups of type 2 diabetic patients, the loss of beta cells as assessed so far might be overestimated, possibly due to changes in beta cell phenotype other than death, also contributing to beta cell failure in type 2 diabetes.</description><subject>Aged</subject><subject>Antibodies</subject><subject>Biological and medical sciences</subject><subject>Chromogranin A - metabolism</subject><subject>Diabetes</subject><subject>Diabetes Mellitus, Type 2 - metabolism</subject><subject>Diabetes Mellitus, Type 2 - pathology</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Etiopathogenesis. Screening. Investigations. Target tissue resistance</subject><subject>Female</subject><subject>Gastrointestinal surgery</subject><subject>Glucagon</subject><subject>Glucagon - metabolism</subject><subject>Glucose</subject><subject>Human Physiology</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Insulin</subject><subject>Insulin - metabolism</subject><subject>Insulin-Secreting Cells - pathology</subject><subject>Internal Medicine</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Metabolic Diseases</subject><subject>Microscopy</subject><subject>Microscopy, Electron</subject><subject>Morphology</subject><subject>Pancreas - pathology</subject><subject>Short Communication</subject><issn>0012-186X</issn><issn>1432-0428</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><recordid>eNp1kEtLxDAQx4Mo7vr4AF4kIIKX6uTVtCcV8QWCFwVvIU2ma6XbrklX8dubZdcHgqfAzG8m__kRssfgmAHokwjAuMqAiUxAWWRijYyZFDwDyYt1Ml60M1bkTyOyFeMLAAgl800y4pILASofk7PzgPQdaf-GAePQTO3QdBM6PCNt-xhpX9MKB0sdtm2kTUeHjxlSTn1jUx3j6Q7ZqG0bcXf1bpPHq8uHi5vs7v769uL8LnNSqiGzlSp1zmThcyG0R-utKMBBCbysPbicM1WAtqrQZe5AMBSuZt5LXkmBlRfb5Gi5dxb613mKaqZNXKSyHfbzaJhKRgCk1gk9-IO-9PPQpXSGSa2Aa6kgUWxJuZAODVibWUjnhw_DwCz0mqVek_SahV4j0sz-avO8mqL_nvjymYDDFWCjs20dbOea-MMVSjLFy8TxJRdTq5tg-BXx398_AWOtjvQ</recordid><startdate>20140201</startdate><enddate>20140201</enddate><creator>Marselli, Lorella</creator><creator>Suleiman, Mara</creator><creator>Masini, Matilde</creator><creator>Campani, Daniela</creator><creator>Bugliani, Marco</creator><creator>Syed, Farooq</creator><creator>Martino, Luisa</creator><creator>Focosi, Daniele</creator><creator>Scatena, Fabrizio</creator><creator>Olimpico, Francesco</creator><creator>Filipponi, Franco</creator><creator>Masiello, Pellegrino</creator><creator>Boggi, Ugo</creator><creator>Marchetti, Piero</creator><general>Springer Berlin Heidelberg</general><general>Springer</general><general>Springer Nature B.V</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20140201</creationdate><title>Are we overestimating the loss of beta cells in type 2 diabetes?</title><author>Marselli, Lorella ; Suleiman, Mara ; Masini, Matilde ; Campani, Daniela ; Bugliani, Marco ; Syed, Farooq ; Martino, Luisa ; Focosi, Daniele ; Scatena, Fabrizio ; Olimpico, Francesco ; Filipponi, Franco ; Masiello, Pellegrino ; Boggi, Ugo ; Marchetti, Piero</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c445t-ab5976148d6337deada380c09029fd0c6215807a58796c031e3cf1dd42b43ebd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Aged</topic><topic>Antibodies</topic><topic>Biological and medical sciences</topic><topic>Chromogranin A - metabolism</topic><topic>Diabetes</topic><topic>Diabetes Mellitus, Type 2 - metabolism</topic><topic>Diabetes Mellitus, Type 2 - pathology</topic><topic>Diabetes. Impaired glucose tolerance</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>Etiopathogenesis. Screening. Investigations. Target tissue resistance</topic><topic>Female</topic><topic>Gastrointestinal surgery</topic><topic>Glucagon</topic><topic>Glucagon - metabolism</topic><topic>Glucose</topic><topic>Human Physiology</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Insulin</topic><topic>Insulin - metabolism</topic><topic>Insulin-Secreting Cells - pathology</topic><topic>Internal Medicine</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Metabolic Diseases</topic><topic>Microscopy</topic><topic>Microscopy, Electron</topic><topic>Morphology</topic><topic>Pancreas - pathology</topic><topic>Short Communication</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Marselli, Lorella</creatorcontrib><creatorcontrib>Suleiman, Mara</creatorcontrib><creatorcontrib>Masini, Matilde</creatorcontrib><creatorcontrib>Campani, Daniela</creatorcontrib><creatorcontrib>Bugliani, Marco</creatorcontrib><creatorcontrib>Syed, Farooq</creatorcontrib><creatorcontrib>Martino, Luisa</creatorcontrib><creatorcontrib>Focosi, Daniele</creatorcontrib><creatorcontrib>Scatena, Fabrizio</creatorcontrib><creatorcontrib>Olimpico, Francesco</creatorcontrib><creatorcontrib>Filipponi, Franco</creatorcontrib><creatorcontrib>Masiello, Pellegrino</creatorcontrib><creatorcontrib>Boggi, Ugo</creatorcontrib><creatorcontrib>Marchetti, Piero</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>ProQuest Health and Medical</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Diabetologia</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Marselli, Lorella</au><au>Suleiman, Mara</au><au>Masini, Matilde</au><au>Campani, Daniela</au><au>Bugliani, Marco</au><au>Syed, Farooq</au><au>Martino, Luisa</au><au>Focosi, Daniele</au><au>Scatena, Fabrizio</au><au>Olimpico, Francesco</au><au>Filipponi, Franco</au><au>Masiello, Pellegrino</au><au>Boggi, Ugo</au><au>Marchetti, Piero</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Are we overestimating the loss of beta cells in type 2 diabetes?</atitle><jtitle>Diabetologia</jtitle><stitle>Diabetologia</stitle><addtitle>Diabetologia</addtitle><date>2014-02-01</date><risdate>2014</risdate><volume>57</volume><issue>2</issue><spage>362</spage><epage>365</epage><pages>362-365</pages><issn>0012-186X</issn><eissn>1432-0428</eissn><abstract>Aims/hypothesis
Previous work has demonstrated that beta cell amount (whether measured as beta cell mass, beta cell volume or insulin-positive area) is decreased in type 2 diabetes; however, recent findings suggest that mechanisms other than death may contribute to beta cell failure in this disease. To better characterise beta cell mass and function in type 2 diabetes, we performed morphological, ultra-structural and functional studies using histological samples and isolated islets.
Methods
Pancreases from ten non-diabetic (ND) and ten matched type 2 diabetic organ donors were studied by insulin, glucagon and chromogranin A immunocytochemistry and electron microscopy (EM). Glucose-stimulated insulin secretion was assessed using isolated islets and studies were performed using independent ND islet preparations after 24 h exposure to 22.2 mmol/l glucose.
Results
Immunocytochemistry showed that the fractional islet insulin-positive area was lower in type 2 diabetic islets (54.9 ± 6.3% vs 72.1 ± 8.7%,
p
< 0.01), whereas glucagon (23.3 ± 5.4% vs 20.2 ± 5.3%) and chromogranin A (86.4 ± 6.1% vs 89.0 ± 5.5%) staining was similar between the two groups. EM showed that the proportion of beta cells in type 2 diabetic islets was only marginally decreased; marked beta cell degranulation was found in diabetic beta cells; these findings were all reproduced after exposing isolated ND islets to high glucose. Glucose-stimulated insulin secretion was 40–50% lower from type 2 diabetic islets (
p
< 0.01), which again was mimicked by culturing non-diabetic islets in high glucose.
Conclusions/interpretation
These results suggest that, at least in subgroups of type 2 diabetic patients, the loss of beta cells as assessed so far might be overestimated, possibly due to changes in beta cell phenotype other than death, also contributing to beta cell failure in type 2 diabetes.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>24233056</pmid><doi>10.1007/s00125-013-3098-3</doi><tpages>4</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Aged Antibodies Biological and medical sciences Chromogranin A - metabolism Diabetes Diabetes Mellitus, Type 2 - metabolism Diabetes Mellitus, Type 2 - pathology Diabetes. Impaired glucose tolerance Endocrine pancreas. Apud cells (diseases) Endocrinopathies Etiopathogenesis. Screening. Investigations. Target tissue resistance Female Gastrointestinal surgery Glucagon Glucagon - metabolism Glucose Human Physiology Humans Immunohistochemistry Insulin Insulin - metabolism Insulin-Secreting Cells - pathology Internal Medicine Male Medical sciences Medicine Medicine & Public Health Metabolic Diseases Microscopy Microscopy, Electron Morphology Pancreas - pathology Short Communication |
| title | Are we overestimating the loss of beta cells in type 2 diabetes? |
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