Epigenetic Regulation in Etiology of Type 1 Diabetes Mellitus
Type 1 diabetes mellitus (T1DM) is caused by an autoimmune destruction of the pancreatic β-cells, a process in which autoreactive T cells play a pivotal role, and it is characterized by islet autoantibodies. Consequent hyperglycemia is requiring lifelong insulin replacement therapy. T1DM is caused b...
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| Veröffentlicht in: | International journal of molecular sciences 2019-12, Vol.21 (1), p.36 |
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| description | Type 1 diabetes mellitus (T1DM) is caused by an autoimmune destruction of the pancreatic β-cells, a process in which autoreactive T cells play a pivotal role, and it is characterized by islet autoantibodies. Consequent hyperglycemia is requiring lifelong insulin replacement therapy. T1DM is caused by the interaction of multiple environmental and genetic factors. The integrations of environments and genes occur via epigenetic regulations of the genome, which allow adaptation of organism to changing life conditions by alternation of gene expression. T1DM has increased several-fold over the past half century. Such a short time indicates involvement of environment factors and excludes genetic changes. This review summarizes the most current knowledge of epigenetic changes in that process leading to autoimmune diabetes mellitus. |
| doi_str_mv | 10.3390/ijms21010036 |
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Consequent hyperglycemia is requiring lifelong insulin replacement therapy. T1DM is caused by the interaction of multiple environmental and genetic factors. The integrations of environments and genes occur via epigenetic regulations of the genome, which allow adaptation of organism to changing life conditions by alternation of gene expression. T1DM has increased several-fold over the past half century. Such a short time indicates involvement of environment factors and excludes genetic changes. This review summarizes the most current knowledge of epigenetic changes in that process leading to autoimmune diabetes mellitus.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms21010036</identifier><identifier>PMID: 31861649</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Antigens ; Autoantibodies ; Autoimmune diseases ; Beta cells ; Binding sites ; Chromosomes ; Diabetes ; Diabetes mellitus ; Diabetes mellitus (insulin dependent) ; Diabetes Mellitus, Type 1 - genetics ; Disease ; DNA methylation ; Epigenesis, Genetic ; Epigenetics ; Etiology ; Fatty acids ; Gene expression ; Gene Expression Regulation ; Gene Regulatory Networks ; Genetic factors ; Genetic Predisposition to Disease ; Genomes ; Health risk assessment ; Humans ; Hyperglycemia ; Hypotheses ; Immune system ; Insulin ; Insulin resistance ; Lymphocytes ; Lymphocytes T ; Pancreas ; Review ; Risk factors ; RNA polymerase ; Transcription factors ; Twins</subject><ispartof>International journal of molecular sciences, 2019-12, Vol.21 (1), p.36</ispartof><rights>2019 by the author. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). 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Consequent hyperglycemia is requiring lifelong insulin replacement therapy. T1DM is caused by the interaction of multiple environmental and genetic factors. The integrations of environments and genes occur via epigenetic regulations of the genome, which allow adaptation of organism to changing life conditions by alternation of gene expression. T1DM has increased several-fold over the past half century. Such a short time indicates involvement of environment factors and excludes genetic changes. This review summarizes the most current knowledge of epigenetic changes in that process leading to autoimmune diabetes mellitus.</description><subject>Antigens</subject><subject>Autoantibodies</subject><subject>Autoimmune diseases</subject><subject>Beta cells</subject><subject>Binding sites</subject><subject>Chromosomes</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diabetes mellitus (insulin dependent)</subject><subject>Diabetes Mellitus, Type 1 - genetics</subject><subject>Disease</subject><subject>DNA methylation</subject><subject>Epigenesis, Genetic</subject><subject>Epigenetics</subject><subject>Etiology</subject><subject>Fatty acids</subject><subject>Gene expression</subject><subject>Gene Expression Regulation</subject><subject>Gene Regulatory Networks</subject><subject>Genetic factors</subject><subject>Genetic Predisposition to Disease</subject><subject>Genomes</subject><subject>Health risk assessment</subject><subject>Humans</subject><subject>Hyperglycemia</subject><subject>Hypotheses</subject><subject>Immune system</subject><subject>Insulin</subject><subject>Insulin resistance</subject><subject>Lymphocytes</subject><subject>Lymphocytes T</subject><subject>Pancreas</subject><subject>Review</subject><subject>Risk factors</subject><subject>RNA polymerase</subject><subject>Transcription factors</subject><subject>Twins</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpdkc1LAzEQxYMotlZvnmXBiwdXM0k22T0oSK0fUBGknsNuOltTtpu62RX63xtpLdXTPJgfj3nzCDkFesV5Rq_tfOEZUKCUyz3SB8FYTKlU-zu6R468n1PKOEuyQ9LjkEqQIuuTm9HSzrDG1proDWddlbfW1ZGto1EQlZutIldGk9USI4jubV5giz56waqybeePyUGZVx5PNnNA3h9Gk-FTPH59fB7ejWMjgLVxIiFLAJHloKYIChUvjTJTxgvIpkaWsuCyKNDQQiTAQJVCmjIxqaKKBc0H5Hbtu-yKBU4N1m2TV3rZ2EXerLTLrf67qe2HnrkvLbMUZJIGg4uNQeM-O_StXlhvQoq8Rtd5HR6TKS5YmgT0_B86d11Th3iaJSKVKs2ECNTlmjKN877BcnsMUP3Ti97tJeBnuwG28G8R_BufHIh8</recordid><startdate>20191219</startdate><enddate>20191219</enddate><creator>Cerna, Marie</creator><general>MDPI AG</general><general>MDPI</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-1208-5588</orcidid></search><sort><creationdate>20191219</creationdate><title>Epigenetic Regulation in Etiology of Type 1 Diabetes Mellitus</title><author>Cerna, Marie</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c412t-561951ee2a17de17e73fc7cd23b19dc6f6b36bbec0b451217f46cf5c87072f463</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Antigens</topic><topic>Autoantibodies</topic><topic>Autoimmune diseases</topic><topic>Beta cells</topic><topic>Binding sites</topic><topic>Chromosomes</topic><topic>Diabetes</topic><topic>Diabetes mellitus</topic><topic>Diabetes mellitus (insulin dependent)</topic><topic>Diabetes Mellitus, Type 1 - genetics</topic><topic>Disease</topic><topic>DNA methylation</topic><topic>Epigenesis, Genetic</topic><topic>Epigenetics</topic><topic>Etiology</topic><topic>Fatty acids</topic><topic>Gene expression</topic><topic>Gene Expression Regulation</topic><topic>Gene Regulatory Networks</topic><topic>Genetic factors</topic><topic>Genetic Predisposition to Disease</topic><topic>Genomes</topic><topic>Health risk assessment</topic><topic>Humans</topic><topic>Hyperglycemia</topic><topic>Hypotheses</topic><topic>Immune system</topic><topic>Insulin</topic><topic>Insulin resistance</topic><topic>Lymphocytes</topic><topic>Lymphocytes T</topic><topic>Pancreas</topic><topic>Review</topic><topic>Risk factors</topic><topic>RNA polymerase</topic><topic>Transcription factors</topic><topic>Twins</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cerna, Marie</creatorcontrib><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>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Publicly Available Content 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>ProQuest Central Basic</collection><collection>MEDLINE - 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| subjects | Antigens Autoantibodies Autoimmune diseases Beta cells Binding sites Chromosomes Diabetes Diabetes mellitus Diabetes mellitus (insulin dependent) Diabetes Mellitus, Type 1 - genetics Disease DNA methylation Epigenesis, Genetic Epigenetics Etiology Fatty acids Gene expression Gene Expression Regulation Gene Regulatory Networks Genetic factors Genetic Predisposition to Disease Genomes Health risk assessment Humans Hyperglycemia Hypotheses Immune system Insulin Insulin resistance Lymphocytes Lymphocytes T Pancreas Review Risk factors RNA polymerase Transcription factors Twins |
| title | Epigenetic Regulation in Etiology of Type 1 Diabetes Mellitus |
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