Islet inflammation: a unifying target for diabetes treatment?
In the past decade, islet inflammation has emerged as a contributor to the loss of functional β cell mass in both type 1 (T1D) and type 2 diabetes (T2D). Evidence supports the idea that overnutrition and insulin resistance result in the production of proinflammatory mediators by β cells. In addition...
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| Veröffentlicht in: | Trends in endocrinology and metabolism 2013-07, Vol.24 (7), p.351-360 |
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| creator | Imai, Yumi Dobrian, Anca D Morris, Margaret A Nadler, Jerry L |
| description | In the past decade, islet inflammation has emerged as a contributor to the loss of functional β cell mass in both type 1 (T1D) and type 2 diabetes (T2D). Evidence supports the idea that overnutrition and insulin resistance result in the production of proinflammatory mediators by β cells. In addition to compromising β cell function and survival, cytokines may recruit macrophages into islets, thus augmenting inflammation. Limited but intriguing data imply a role of adaptive immune response in islet dysfunction in T2D. Clinical trials have validated anti-inflammatory therapies in T2D, whereas immune therapy for T1D remains challenging. Further research is required to improve our understanding of islet inflammatory pathways and to identify more effective therapeutic targets for T1D and T2D. |
| doi_str_mv | 10.1016/j.tem.2013.01.007 |
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Evidence supports the idea that overnutrition and insulin resistance result in the production of proinflammatory mediators by β cells. In addition to compromising β cell function and survival, cytokines may recruit macrophages into islets, thus augmenting inflammation. Limited but intriguing data imply a role of adaptive immune response in islet dysfunction in T2D. Clinical trials have validated anti-inflammatory therapies in T2D, whereas immune therapy for T1D remains challenging. Further research is required to improve our understanding of islet inflammatory pathways and to identify more effective therapeutic targets for T1D and T2D.</description><identifier>ISSN: 1043-2760</identifier><identifier>EISSN: 1879-3061</identifier><identifier>DOI: 10.1016/j.tem.2013.01.007</identifier><identifier>PMID: 23484621</identifier><language>eng</language><publisher>United States: Elsevier Ltd</publisher><subject>adipocyte ; Animals ; Anti-Inflammatory Agents - pharmacology ; Anti-Inflammatory Agents - therapeutic use ; clinical trials ; cytokine ; Diabetes Mellitus, Type 1 - drug therapy ; Diabetes Mellitus, Type 1 - immunology ; Diabetes Mellitus, Type 1 - metabolism ; Diabetes Mellitus, Type 2 - drug therapy ; Diabetes Mellitus, Type 2 - immunology ; Diabetes Mellitus, Type 2 - metabolism ; Endocrinology & Metabolism ; Endoplasmic Reticulum Stress - drug effects ; Humans ; Hypoglycemic Agents - pharmacology ; Hypoglycemic Agents - therapeutic use ; immune cells ; Inflammation Mediators - metabolism ; Insulin Resistance ; Islet Amyloid Polypeptide - metabolism ; Islet Amyloid Polypeptide - secretion ; Islets of Langerhans - drug effects ; Islets of Langerhans - immunology ; Islets of Langerhans - metabolism ; Islets of Langerhans - secretion ; Macrophages - drug effects ; Macrophages - immunology ; Macrophages - metabolism ; Macrophages - secretion ; Molecular Targeted Therapy ; obesity ; β cell</subject><ispartof>Trends in endocrinology and metabolism, 2013-07, Vol.24 (7), p.351-360</ispartof><rights>Elsevier Ltd</rights><rights>2013 Elsevier Ltd</rights><rights>Copyright © 2013 Elsevier Ltd. All rights reserved.</rights><rights>2013 Elsevier Ltd. All rights reserved. 2013</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c506t-c3c139214fed8bb5a9ba01becf713712914524dcbb7b3831550122f9b885bfba3</citedby><cites>FETCH-LOGICAL-c506t-c3c139214fed8bb5a9ba01becf713712914524dcbb7b3831550122f9b885bfba3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.tem.2013.01.007$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,780,784,885,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23484621$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Imai, Yumi</creatorcontrib><creatorcontrib>Dobrian, Anca D</creatorcontrib><creatorcontrib>Morris, Margaret A</creatorcontrib><creatorcontrib>Nadler, Jerry L</creatorcontrib><title>Islet inflammation: a unifying target for diabetes treatment?</title><title>Trends in endocrinology and metabolism</title><addtitle>Trends Endocrinol Metab</addtitle><description>In the past decade, islet inflammation has emerged as a contributor to the loss of functional β cell mass in both type 1 (T1D) and type 2 diabetes (T2D). Evidence supports the idea that overnutrition and insulin resistance result in the production of proinflammatory mediators by β cells. In addition to compromising β cell function and survival, cytokines may recruit macrophages into islets, thus augmenting inflammation. Limited but intriguing data imply a role of adaptive immune response in islet dysfunction in T2D. Clinical trials have validated anti-inflammatory therapies in T2D, whereas immune therapy for T1D remains challenging. Further research is required to improve our understanding of islet inflammatory pathways and to identify more effective therapeutic targets for T1D and T2D.</description><subject>adipocyte</subject><subject>Animals</subject><subject>Anti-Inflammatory Agents - pharmacology</subject><subject>Anti-Inflammatory Agents - therapeutic use</subject><subject>clinical trials</subject><subject>cytokine</subject><subject>Diabetes Mellitus, Type 1 - drug therapy</subject><subject>Diabetes Mellitus, Type 1 - immunology</subject><subject>Diabetes Mellitus, Type 1 - metabolism</subject><subject>Diabetes Mellitus, Type 2 - drug therapy</subject><subject>Diabetes Mellitus, Type 2 - immunology</subject><subject>Diabetes Mellitus, Type 2 - metabolism</subject><subject>Endocrinology & Metabolism</subject><subject>Endoplasmic Reticulum Stress - drug effects</subject><subject>Humans</subject><subject>Hypoglycemic Agents - pharmacology</subject><subject>Hypoglycemic Agents - therapeutic use</subject><subject>immune cells</subject><subject>Inflammation Mediators - metabolism</subject><subject>Insulin Resistance</subject><subject>Islet Amyloid Polypeptide - metabolism</subject><subject>Islet Amyloid Polypeptide - secretion</subject><subject>Islets of Langerhans - drug effects</subject><subject>Islets of Langerhans - immunology</subject><subject>Islets of Langerhans - metabolism</subject><subject>Islets of Langerhans - secretion</subject><subject>Macrophages - drug effects</subject><subject>Macrophages - immunology</subject><subject>Macrophages - metabolism</subject><subject>Macrophages - secretion</subject><subject>Molecular Targeted Therapy</subject><subject>obesity</subject><subject>β cell</subject><issn>1043-2760</issn><issn>1879-3061</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kc1v1DAQxSMEoqXwB3BBOXLJMmPnwwHRClV8VKrEATiPbGeyeEmcYjuV9r_Hqy0VcOBkS_Pem9HvFcVzhA0Ctq92m8TzRgDKDeAGoHtQnKLq-kpCiw_zH2pZia6Fk-JJjDsArBU2j4sTIWtVtwJPi7dXceJUOj9Oep51cot_Xepy9W7cO78tkw7bPB-XUA5OG04cyxRYp5l9unhaPBr1FPnZ3XtWfPvw_uvlp-r688ery3fXlW2gTZWVFmUvsB55UMY0ujca0LAdO5Qdih7rRtSDNaYzUklsGkAhxt4o1ZjRaHlWnB9zb1Yz82Dz7qAnuglu1mFPi3b098S777Rdbkm2qlW1ygEv7wLC8nPlmGh20fI0ac_LGimfIaBTUmGW4lFqwxJj4PF-DQIdsNOOMnY6YCdAytiz58Wf9907fnPOgjdHAWdKt44DRevYWx5cYJtoWNx_48__cdvJeWf19IP3HHfLGnzGT0hRENCXQ--H2lFC7rwX8hfTJahl</recordid><startdate>20130701</startdate><enddate>20130701</enddate><creator>Imai, Yumi</creator><creator>Dobrian, Anca D</creator><creator>Morris, Margaret A</creator><creator>Nadler, Jerry L</creator><general>Elsevier Ltd</general><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>7X8</scope><scope>5PM</scope></search><sort><creationdate>20130701</creationdate><title>Islet inflammation: a unifying target for diabetes treatment?</title><author>Imai, Yumi ; Dobrian, Anca D ; Morris, Margaret A ; Nadler, Jerry L</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c506t-c3c139214fed8bb5a9ba01becf713712914524dcbb7b3831550122f9b885bfba3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>adipocyte</topic><topic>Animals</topic><topic>Anti-Inflammatory Agents - pharmacology</topic><topic>Anti-Inflammatory Agents - therapeutic use</topic><topic>clinical trials</topic><topic>cytokine</topic><topic>Diabetes Mellitus, Type 1 - drug therapy</topic><topic>Diabetes Mellitus, Type 1 - immunology</topic><topic>Diabetes Mellitus, Type 1 - metabolism</topic><topic>Diabetes Mellitus, Type 2 - drug therapy</topic><topic>Diabetes Mellitus, Type 2 - immunology</topic><topic>Diabetes Mellitus, Type 2 - metabolism</topic><topic>Endocrinology & Metabolism</topic><topic>Endoplasmic Reticulum Stress - drug effects</topic><topic>Humans</topic><topic>Hypoglycemic Agents - pharmacology</topic><topic>Hypoglycemic Agents - therapeutic use</topic><topic>immune cells</topic><topic>Inflammation Mediators - metabolism</topic><topic>Insulin Resistance</topic><topic>Islet Amyloid Polypeptide - metabolism</topic><topic>Islet Amyloid Polypeptide - secretion</topic><topic>Islets of Langerhans - drug effects</topic><topic>Islets of Langerhans - immunology</topic><topic>Islets of Langerhans - metabolism</topic><topic>Islets of Langerhans - secretion</topic><topic>Macrophages - drug effects</topic><topic>Macrophages - immunology</topic><topic>Macrophages - metabolism</topic><topic>Macrophages - secretion</topic><topic>Molecular Targeted Therapy</topic><topic>obesity</topic><topic>β cell</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Imai, Yumi</creatorcontrib><creatorcontrib>Dobrian, Anca D</creatorcontrib><creatorcontrib>Morris, Margaret A</creatorcontrib><creatorcontrib>Nadler, Jerry L</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Trends in endocrinology and metabolism</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Imai, Yumi</au><au>Dobrian, Anca D</au><au>Morris, Margaret A</au><au>Nadler, Jerry L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Islet inflammation: a unifying target for diabetes treatment?</atitle><jtitle>Trends in endocrinology and metabolism</jtitle><addtitle>Trends Endocrinol Metab</addtitle><date>2013-07-01</date><risdate>2013</risdate><volume>24</volume><issue>7</issue><spage>351</spage><epage>360</epage><pages>351-360</pages><issn>1043-2760</issn><eissn>1879-3061</eissn><abstract>In the past decade, islet inflammation has emerged as a contributor to the loss of functional β cell mass in both type 1 (T1D) and type 2 diabetes (T2D). Evidence supports the idea that overnutrition and insulin resistance result in the production of proinflammatory mediators by β cells. In addition to compromising β cell function and survival, cytokines may recruit macrophages into islets, thus augmenting inflammation. Limited but intriguing data imply a role of adaptive immune response in islet dysfunction in T2D. Clinical trials have validated anti-inflammatory therapies in T2D, whereas immune therapy for T1D remains challenging. Further research is required to improve our understanding of islet inflammatory pathways and to identify more effective therapeutic targets for T1D and T2D.</abstract><cop>United States</cop><pub>Elsevier Ltd</pub><pmid>23484621</pmid><doi>10.1016/j.tem.2013.01.007</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | adipocyte Animals Anti-Inflammatory Agents - pharmacology Anti-Inflammatory Agents - therapeutic use clinical trials cytokine Diabetes Mellitus, Type 1 - drug therapy Diabetes Mellitus, Type 1 - immunology Diabetes Mellitus, Type 1 - metabolism Diabetes Mellitus, Type 2 - drug therapy Diabetes Mellitus, Type 2 - immunology Diabetes Mellitus, Type 2 - metabolism Endocrinology & Metabolism Endoplasmic Reticulum Stress - drug effects Humans Hypoglycemic Agents - pharmacology Hypoglycemic Agents - therapeutic use immune cells Inflammation Mediators - metabolism Insulin Resistance Islet Amyloid Polypeptide - metabolism Islet Amyloid Polypeptide - secretion Islets of Langerhans - drug effects Islets of Langerhans - immunology Islets of Langerhans - metabolism Islets of Langerhans - secretion Macrophages - drug effects Macrophages - immunology Macrophages - metabolism Macrophages - secretion Molecular Targeted Therapy obesity β cell |
| title | Islet inflammation: a unifying target for diabetes treatment? |
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