Role of the TLR signaling molecule TRIF in β-cell function and glucose homeostasis
Type 2 diabetes is a metabolic and inflammatory disease characterized by deteriorating islet function and increased levels of inflammatory cytokines. The inflammatory milieu induced in type 2 diabetes exacerbates islet dysfunction and insulin resistance, and therapies that target inflammation can im...
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| Veröffentlicht in: | Islets 2010-03, Vol.2 (2), p.104-111 |
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| creator | Hutton, Meredith J. H. Soukhatcheva, Galina Johnson, James D. Verchere, C. Bruce |
| description | Type 2 diabetes is a metabolic and inflammatory disease characterized by deteriorating islet function and increased levels of inflammatory cytokines. The inflammatory milieu induced in type 2 diabetes exacerbates islet dysfunction and insulin resistance, and therapies that target inflammation can improve glycemic control in patients with type 2 diabetes. Inflammation in type 2 diabetes may be the result of the stimulation of Toll-like receptors (TLRs), one of the many mediators of inflammation. TLRs can be activated by both exogenous and endogenous ligands, and are responsible for activating NF-κB and interferon-inducible inflammatory gene expression. We examined the role of the TIR-domain containing adaptor-inducing interferon-β (TRIF or TICAM-1), a major signaling molecule for TLR3 and TLR4, in βa-cell function and glucose homeostasis by examining mice lacking TRIF (Trif
-/-
), TLR3 (Tlr3
-/-
) or TLR4 (Tlr4
-/-
).
Male, 10-week old Trif
-/-
mice exhibit a moderate but significant increase in fasting blood glucose compared to C57BL/6 controls (12.0±0.9 vs. 9.7±0.4 mM; p |
| doi_str_mv | 10.4161/isl.2.2.11209 |
| format | Article |
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-/-
), TLR3 (Tlr3
-/-
) or TLR4 (Tlr4
-/-
).
Male, 10-week old Trif
-/-
mice exhibit a moderate but significant increase in fasting blood glucose compared to C57BL/6 controls (12.0±0.9 vs. 9.7±0.4 mM; p</description><identifier>ISSN: 1938-2014</identifier><identifier>EISSN: 1938-2022</identifier><identifier>DOI: 10.4161/isl.2.2.11209</identifier><identifier>PMID: 21099302</identifier><language>eng</language><publisher>United States: Taylor & Francis</publisher><subject>Adaptor Proteins, Vesicular Transport - genetics ; Adaptor Proteins, Vesicular Transport - metabolism ; Adaptor Proteins, Vesicular Transport - physiology ; Animals ; Binding ; Biology ; Bioscience ; Calcium ; Cancer ; Cell ; Cycle ; Glucose - metabolism ; Glucose Intolerance - genetics ; Glucose Intolerance - metabolism ; Homeostasis - genetics ; Homeostasis - physiology ; Insulin Resistance - genetics ; Insulin Resistance - physiology ; Insulin-Secreting Cells - cytology ; Insulin-Secreting Cells - metabolism ; Insulin-Secreting Cells - physiology ; Landes ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Organ Size - genetics ; Organogenesis ; Pancreas - anatomy & histology ; Pancreas - cytology ; Pancreas - metabolism ; Proteins ; Signal Transduction - genetics ; Signal Transduction - physiology ; Toll-Like Receptors - genetics ; Toll-Like Receptors - metabolism ; Toll-Like Receptors - physiology</subject><ispartof>Islets, 2010-03, Vol.2 (2), p.104-111</ispartof><rights>Copyright © 2010 Landes Bioscience 2010</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c539t-cad91266a66700de4bee3d679f4fa33ffe558262150e4c6055963fb33a6893283</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21099302$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hutton, Meredith J. H.</creatorcontrib><creatorcontrib>Soukhatcheva, Galina</creatorcontrib><creatorcontrib>Johnson, James D.</creatorcontrib><creatorcontrib>Verchere, C. Bruce</creatorcontrib><title>Role of the TLR signaling molecule TRIF in β-cell function and glucose homeostasis</title><title>Islets</title><addtitle>Islets</addtitle><description>Type 2 diabetes is a metabolic and inflammatory disease characterized by deteriorating islet function and increased levels of inflammatory cytokines. The inflammatory milieu induced in type 2 diabetes exacerbates islet dysfunction and insulin resistance, and therapies that target inflammation can improve glycemic control in patients with type 2 diabetes. Inflammation in type 2 diabetes may be the result of the stimulation of Toll-like receptors (TLRs), one of the many mediators of inflammation. TLRs can be activated by both exogenous and endogenous ligands, and are responsible for activating NF-κB and interferon-inducible inflammatory gene expression. We examined the role of the TIR-domain containing adaptor-inducing interferon-β (TRIF or TICAM-1), a major signaling molecule for TLR3 and TLR4, in βa-cell function and glucose homeostasis by examining mice lacking TRIF (Trif
-/-
), TLR3 (Tlr3
-/-
) or TLR4 (Tlr4
-/-
).
Male, 10-week old Trif
-/-
mice exhibit a moderate but significant increase in fasting blood glucose compared to C57BL/6 controls (12.0±0.9 vs. 9.7±0.4 mM; p</description><subject>Adaptor Proteins, Vesicular Transport - genetics</subject><subject>Adaptor Proteins, Vesicular Transport - metabolism</subject><subject>Adaptor Proteins, Vesicular Transport - physiology</subject><subject>Animals</subject><subject>Binding</subject><subject>Biology</subject><subject>Bioscience</subject><subject>Calcium</subject><subject>Cancer</subject><subject>Cell</subject><subject>Cycle</subject><subject>Glucose - metabolism</subject><subject>Glucose Intolerance - genetics</subject><subject>Glucose Intolerance - metabolism</subject><subject>Homeostasis - genetics</subject><subject>Homeostasis - physiology</subject><subject>Insulin Resistance - genetics</subject><subject>Insulin Resistance - physiology</subject><subject>Insulin-Secreting Cells - cytology</subject><subject>Insulin-Secreting Cells - metabolism</subject><subject>Insulin-Secreting Cells - physiology</subject><subject>Landes</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Organ Size - genetics</subject><subject>Organogenesis</subject><subject>Pancreas - anatomy & histology</subject><subject>Pancreas - cytology</subject><subject>Pancreas - metabolism</subject><subject>Proteins</subject><subject>Signal Transduction - genetics</subject><subject>Signal Transduction - physiology</subject><subject>Toll-Like Receptors - genetics</subject><subject>Toll-Like Receptors - metabolism</subject><subject>Toll-Like Receptors - physiology</subject><issn>1938-2014</issn><issn>1938-2022</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>0YH</sourceid><sourceid>EIF</sourceid><recordid>eNqFkE1qHDEUhJsQEztOltkG7bJqW38tt5bB2PHAgGHcWQuN-mmsoJYmkprg2_gMOUIOkDNF43FmZTBvIcH7qlSqpvlE8Bkngpy77M9oHUIolm-aEyJZ31JM6dvDnfDj5n3OPzAWkmL-rjmmBEvJMD1phlX0gKJF5R7QsFyh7DZBexc2aKobM9ftsFpcIxf-PP793RrwHtk5mOJiQDqMaONnEzOg-zhBzEVnlz80R1b7DB-fz9Pm-_XVcHnTLm-_LS6_LlvTMVlao0dJqBBaiAuMR-BrADaKC2m51YxZC13XU0FJh4EbgbtOCmbXjGnRS0Z7dtp82ftuU_w5Qy5qcnmXUAeIc1Y9oYRxzmkl2z1pUsw5gVXb5CadHhTBatejqj0qWuepx8p_fnae1xOMB_p_cRVge6C-NUJeu5iNg2DggN7MpcSwuFteDXc74-1oq4q_oqoxoGSlU3HGwyFNv5e5YGOa9K-Y_KiKfvAx2aSDcVmxlz_yD742qHk</recordid><startdate>20100301</startdate><enddate>20100301</enddate><creator>Hutton, Meredith J. 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TLRs can be activated by both exogenous and endogenous ligands, and are responsible for activating NF-κB and interferon-inducible inflammatory gene expression. We examined the role of the TIR-domain containing adaptor-inducing interferon-β (TRIF or TICAM-1), a major signaling molecule for TLR3 and TLR4, in βa-cell function and glucose homeostasis by examining mice lacking TRIF (Trif
-/-
), TLR3 (Tlr3
-/-
) or TLR4 (Tlr4
-/-
).
Male, 10-week old Trif
-/-
mice exhibit a moderate but significant increase in fasting blood glucose compared to C57BL/6 controls (12.0±0.9 vs. 9.7±0.4 mM; p</abstract><cop>United States</cop><pub>Taylor & Francis</pub><pmid>21099302</pmid><doi>10.4161/isl.2.2.11209</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; EZB-FREE-00999 freely available EZB journals; PubMed Central |
| subjects | Adaptor Proteins, Vesicular Transport - genetics Adaptor Proteins, Vesicular Transport - metabolism Adaptor Proteins, Vesicular Transport - physiology Animals Binding Biology Bioscience Calcium Cancer Cell Cycle Glucose - metabolism Glucose Intolerance - genetics Glucose Intolerance - metabolism Homeostasis - genetics Homeostasis - physiology Insulin Resistance - genetics Insulin Resistance - physiology Insulin-Secreting Cells - cytology Insulin-Secreting Cells - metabolism Insulin-Secreting Cells - physiology Landes Male Mice Mice, Inbred C57BL Mice, Knockout Organ Size - genetics Organogenesis Pancreas - anatomy & histology Pancreas - cytology Pancreas - metabolism Proteins Signal Transduction - genetics Signal Transduction - physiology Toll-Like Receptors - genetics Toll-Like Receptors - metabolism Toll-Like Receptors - physiology |
| title | Role of the TLR signaling molecule TRIF in β-cell function and glucose homeostasis |
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