Minireview: Epigenetic Programming of Diabetes and Obesity: Animal Models
A growing body of evidence suggests that the intrauterine (IU) environment has a significant and lasting effect on the long-term health of the growing fetus and the development of metabolic disease in later life as put forth in the fetal origins of disease hypothesis. Metabolic diseases have been as...
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| Veröffentlicht in: | Endocrinology (Philadelphia) 2012-03, Vol.153 (3), p.1031-1038 |
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| description | A growing body of evidence suggests that the intrauterine (IU) environment has a significant and lasting effect on the long-term health of the growing fetus and the development of metabolic disease in later life as put forth in the fetal origins of disease hypothesis. Metabolic diseases have been associated with alterations in the epigenome that occur without changes in the DNA sequence, such as cytosine methylation of DNA, histone posttranslational modifications, and micro-RNA. Animal models of epigenetic modifications secondary to an altered IU milieu are an invaluable tool to study the mechanisms that determine the development of metabolic diseases, such as diabetes and obesity. Rodent and nonlitter bearing animals are good models for the study of disease, because they have similar embryology, anatomy, and physiology to humans. Thus, it is feasible to monitor and modify the IU environment of animal models in order to gain insight into the molecular basis of human metabolic disease pathogenesis. In this review, the database of PubMed was searched for articles published between 1999 and 2011. Key words included epigenetic modifications, IU growth retardation, small for gestational age, animal models, metabolic disease, and obesity. The inclusion criteria used to select studies included animal models of epigenetic modifications during fetal and neonatal development associated with adult metabolic syndrome. Experimental manipulations included: changes in the nutritional status of the pregnant female (calorie-restricted, high-fat, or low-protein diets during pregnancy), as well as the father; interference with placenta function, or uterine blood flow, environmental toxin exposure during pregnancy, as well as dietary modifications during the neonatal (lactation) as well as pubertal period. This review article is focused solely on studies in animal models that demonstrate epigenetic changes that are correlated with manifestation of metabolic disease, including diabetes and/or obesity. |
| doi_str_mv | 10.1210/en.2011-1805 |
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Metabolic diseases have been associated with alterations in the epigenome that occur without changes in the DNA sequence, such as cytosine methylation of DNA, histone posttranslational modifications, and micro-RNA. Animal models of epigenetic modifications secondary to an altered IU milieu are an invaluable tool to study the mechanisms that determine the development of metabolic diseases, such as diabetes and obesity. Rodent and nonlitter bearing animals are good models for the study of disease, because they have similar embryology, anatomy, and physiology to humans. Thus, it is feasible to monitor and modify the IU environment of animal models in order to gain insight into the molecular basis of human metabolic disease pathogenesis. In this review, the database of PubMed was searched for articles published between 1999 and 2011. Key words included epigenetic modifications, IU growth retardation, small for gestational age, animal models, metabolic disease, and obesity. The inclusion criteria used to select studies included animal models of epigenetic modifications during fetal and neonatal development associated with adult metabolic syndrome. Experimental manipulations included: changes in the nutritional status of the pregnant female (calorie-restricted, high-fat, or low-protein diets during pregnancy), as well as the father; interference with placenta function, or uterine blood flow, environmental toxin exposure during pregnancy, as well as dietary modifications during the neonatal (lactation) as well as pubertal period. This review article is focused solely on studies in animal models that demonstrate epigenetic changes that are correlated with manifestation of metabolic disease, including diabetes and/or obesity.</description><identifier>ISSN: 0013-7227</identifier><identifier>EISSN: 1945-7170</identifier><identifier>DOI: 10.1210/en.2011-1805</identifier><identifier>PMID: 22253432</identifier><identifier>CODEN: ENDOAO</identifier><language>eng</language><publisher>Chevy Chase, MD: Endocrine Society</publisher><subject>Animal diseases ; Animal models ; Animals ; Biological and medical sciences ; Blood flow ; Cytosine ; Deoxyribonucleic acid ; Diabetes ; Diabetes mellitus ; Diabetes Mellitus - genetics ; Diabetes. Impaired glucose tolerance ; Disease ; Disease Models, Animal ; DNA ; DNA Methylation ; Embryology ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Environmental monitoring ; Epigenesis, Genetic ; Epigenetics ; Etiopathogenesis. Screening. Investigations. Target tissue resistance ; Female ; Fetuses ; Forth (programming language) ; Fundamental and applied biological sciences. Psychology ; Gestational age ; Growth rate ; High fat diet ; High protein diet ; Histones ; Humans ; Intrauterine exposure ; Lactation ; Low fat diet ; Male ; Medical sciences ; Metabolic diseases ; Metabolic disorders ; Metabolic syndrome ; Mice ; Mice, Inbred C57BL ; Minireviews ; Molecular modelling ; Neonates ; Nucleotide sequence ; Nutrient deficiency ; Nutritional status ; Obesity ; Obesity - genetics ; Pathogenesis ; Placenta ; Placenta - metabolism ; Pregnancy ; PubMed ; Rats ; RNA, Messenger - metabolism ; Toxins ; Vertebrates: endocrinology</subject><ispartof>Endocrinology (Philadelphia), 2012-03, Vol.153 (3), p.1031-1038</ispartof><rights>Copyright © 2012 by The Endocrine Society</rights><rights>Copyright © 2012 by The Endocrine Society 2012</rights><rights>2015 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c616t-9f9c2a1b5313492044ddfd3b272df3be9b9e72c0c8a9375581d1d1fa59730cfd3</citedby><cites>FETCH-LOGICAL-c616t-9f9c2a1b5313492044ddfd3b272df3be9b9e72c0c8a9375581d1d1fa59730cfd3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,315,781,785,886,27928,27929</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=25544394$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22253432$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Seki, Yoshinori</creatorcontrib><creatorcontrib>Williams, Lyda</creatorcontrib><creatorcontrib>Vuguin, Patricia M</creatorcontrib><creatorcontrib>Charron, Maureen J</creatorcontrib><title>Minireview: Epigenetic Programming of Diabetes and Obesity: Animal Models</title><title>Endocrinology (Philadelphia)</title><addtitle>Endocrinology</addtitle><description>A growing body of evidence suggests that the intrauterine (IU) environment has a significant and lasting effect on the long-term health of the growing fetus and the development of metabolic disease in later life as put forth in the fetal origins of disease hypothesis. Metabolic diseases have been associated with alterations in the epigenome that occur without changes in the DNA sequence, such as cytosine methylation of DNA, histone posttranslational modifications, and micro-RNA. Animal models of epigenetic modifications secondary to an altered IU milieu are an invaluable tool to study the mechanisms that determine the development of metabolic diseases, such as diabetes and obesity. Rodent and nonlitter bearing animals are good models for the study of disease, because they have similar embryology, anatomy, and physiology to humans. Thus, it is feasible to monitor and modify the IU environment of animal models in order to gain insight into the molecular basis of human metabolic disease pathogenesis. In this review, the database of PubMed was searched for articles published between 1999 and 2011. Key words included epigenetic modifications, IU growth retardation, small for gestational age, animal models, metabolic disease, and obesity. The inclusion criteria used to select studies included animal models of epigenetic modifications during fetal and neonatal development associated with adult metabolic syndrome. Experimental manipulations included: changes in the nutritional status of the pregnant female (calorie-restricted, high-fat, or low-protein diets during pregnancy), as well as the father; interference with placenta function, or uterine blood flow, environmental toxin exposure during pregnancy, as well as dietary modifications during the neonatal (lactation) as well as pubertal period. This review article is focused solely on studies in animal models that demonstrate epigenetic changes that are correlated with manifestation of metabolic disease, including diabetes and/or obesity.</description><subject>Animal diseases</subject><subject>Animal models</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Blood flow</subject><subject>Cytosine</subject><subject>Deoxyribonucleic acid</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diabetes Mellitus - genetics</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Disease</subject><subject>Disease Models, Animal</subject><subject>DNA</subject><subject>DNA Methylation</subject><subject>Embryology</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Environmental monitoring</subject><subject>Epigenesis, Genetic</subject><subject>Epigenetics</subject><subject>Etiopathogenesis. Screening. Investigations. Target tissue resistance</subject><subject>Female</subject><subject>Fetuses</subject><subject>Forth (programming language)</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gestational age</subject><subject>Growth rate</subject><subject>High fat diet</subject><subject>High protein diet</subject><subject>Histones</subject><subject>Humans</subject><subject>Intrauterine exposure</subject><subject>Lactation</subject><subject>Low fat diet</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Metabolic diseases</subject><subject>Metabolic disorders</subject><subject>Metabolic syndrome</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Minireviews</subject><subject>Molecular modelling</subject><subject>Neonates</subject><subject>Nucleotide sequence</subject><subject>Nutrient deficiency</subject><subject>Nutritional status</subject><subject>Obesity</subject><subject>Obesity - genetics</subject><subject>Pathogenesis</subject><subject>Placenta</subject><subject>Placenta - metabolism</subject><subject>Pregnancy</subject><subject>PubMed</subject><subject>Rats</subject><subject>RNA, Messenger - metabolism</subject><subject>Toxins</subject><subject>Vertebrates: endocrinology</subject><issn>0013-7227</issn><issn>1945-7170</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kc9rFDEYhoNU7Lr25rkMFNGDU_Njspn0IJRabaGlHuo5ZJJvtikzyTSZqfS_N8OurUolhxDy8H3vy4PQW4IPCSX4E_hDigkpSY35C7QgsuKlIALvoAXGhJWCUrGLXqd0m59VVbFXaJdSylnF6AKdXzrvItw7-HlUnA5uDR5GZ4rvMayj7nvn10Voiy9ONzBCKrS3xVUDyY0PR8Wxd73uistgoUtv0MtWdwn2tvcS_fh6en1yVl5cfTs_Ob4ozYqsxlK20lBNGs4IqyTFVWVta1lDBbUta0A2EgQ12NRaMsF5TWw-reZSMGwyuUSfN3OHqenBGvBj1J0aYs4SH1TQTv39492NWod7xWhN5tZL9GE7IIa7CdKoepcMdJ32EKakCMZ1zRhf8Ywe_IPehin6XE_l-HhFseAsUx83lIkhpQjtYxiC1exIgVezIzU7yvj-nwUe4d9SMvBuC-hkdNdG7Y1LTxzn2aKci7zfcGEa_rey3K5kGxK8DSY6D0OElJ7aPBv0F8zytc8</recordid><startdate>20120301</startdate><enddate>20120301</enddate><creator>Seki, Yoshinori</creator><creator>Williams, Lyda</creator><creator>Vuguin, Patricia M</creator><creator>Charron, Maureen J</creator><general>Endocrine Society</general><general>Oxford University Press</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>7QG</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7TM</scope><scope>7TO</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>7TS</scope><scope>5PM</scope></search><sort><creationdate>20120301</creationdate><title>Minireview: Epigenetic Programming of Diabetes and Obesity: Animal Models</title><author>Seki, Yoshinori ; Williams, Lyda ; Vuguin, Patricia M ; Charron, Maureen J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c616t-9f9c2a1b5313492044ddfd3b272df3be9b9e72c0c8a9375581d1d1fa59730cfd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Animal diseases</topic><topic>Animal models</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Blood flow</topic><topic>Cytosine</topic><topic>Deoxyribonucleic acid</topic><topic>Diabetes</topic><topic>Diabetes mellitus</topic><topic>Diabetes Mellitus - genetics</topic><topic>Diabetes. 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Metabolic diseases have been associated with alterations in the epigenome that occur without changes in the DNA sequence, such as cytosine methylation of DNA, histone posttranslational modifications, and micro-RNA. Animal models of epigenetic modifications secondary to an altered IU milieu are an invaluable tool to study the mechanisms that determine the development of metabolic diseases, such as diabetes and obesity. Rodent and nonlitter bearing animals are good models for the study of disease, because they have similar embryology, anatomy, and physiology to humans. Thus, it is feasible to monitor and modify the IU environment of animal models in order to gain insight into the molecular basis of human metabolic disease pathogenesis. In this review, the database of PubMed was searched for articles published between 1999 and 2011. Key words included epigenetic modifications, IU growth retardation, small for gestational age, animal models, metabolic disease, and obesity. The inclusion criteria used to select studies included animal models of epigenetic modifications during fetal and neonatal development associated with adult metabolic syndrome. Experimental manipulations included: changes in the nutritional status of the pregnant female (calorie-restricted, high-fat, or low-protein diets during pregnancy), as well as the father; interference with placenta function, or uterine blood flow, environmental toxin exposure during pregnancy, as well as dietary modifications during the neonatal (lactation) as well as pubertal period. This review article is focused solely on studies in animal models that demonstrate epigenetic changes that are correlated with manifestation of metabolic disease, including diabetes and/or obesity.</abstract><cop>Chevy Chase, MD</cop><pub>Endocrine Society</pub><pmid>22253432</pmid><doi>10.1210/en.2011-1805</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animal diseases Animal models Animals Biological and medical sciences Blood flow Cytosine Deoxyribonucleic acid Diabetes Diabetes mellitus Diabetes Mellitus - genetics Diabetes. Impaired glucose tolerance Disease Disease Models, Animal DNA DNA Methylation Embryology Endocrine pancreas. Apud cells (diseases) Endocrinopathies Environmental monitoring Epigenesis, Genetic Epigenetics Etiopathogenesis. Screening. Investigations. Target tissue resistance Female Fetuses Forth (programming language) Fundamental and applied biological sciences. Psychology Gestational age Growth rate High fat diet High protein diet Histones Humans Intrauterine exposure Lactation Low fat diet Male Medical sciences Metabolic diseases Metabolic disorders Metabolic syndrome Mice Mice, Inbred C57BL Minireviews Molecular modelling Neonates Nucleotide sequence Nutrient deficiency Nutritional status Obesity Obesity - genetics Pathogenesis Placenta Placenta - metabolism Pregnancy PubMed Rats RNA, Messenger - metabolism Toxins Vertebrates: endocrinology |
| title | Minireview: Epigenetic Programming of Diabetes and Obesity: Animal Models |
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