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Diabetes consequences in the fetus liver of the non-obese diabetic mice
DM type 1 (T1D) incidence is increasing around 3% every year and represents risks for maternal and fetal health. The objective of this study was to explore the effects of diabetes on fetus liver cells in non-obese diabetic (NOD) mice. Hyperglycemic NOD (HNOD), normoglycemic NOD (NNOD) and BALB/c fem...
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| Published in: | Nutrition & diabetes 2017-03, Vol.7 (3), p.e257-e257 |
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| container_end_page | e257 |
| container_issue | 3 |
| container_start_page | e257 |
| container_title | Nutrition & diabetes |
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| creator | Aires, M B dos Santos, A C V Kubrusly, M S de Lima Luna, A C D’Albuquerque, L A C Maria, D A |
| description | DM type 1 (T1D) incidence is increasing around 3% every year and represents risks for maternal and fetal health. The objective of this study was to explore the effects of diabetes on fetus liver cells in non-obese diabetic (NOD) mice. Hyperglycemic NOD (HNOD), normoglycemic NOD (NNOD) and BALB/c females were used for mating, and the fetus livers were collected at 19.5 gestation day (gd). HNOD group had reduced fetal weight (989.5±68.32 vs 1290±57.39 mg BALB/c,
P |
| doi_str_mv | 10.1038/nutd.2017.7 |
| format | article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5380899</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>4321996209</sourcerecordid><originalsourceid>FETCH-LOGICAL-c404t-1f44e9247512b6807c495a6867dca126e735facaac80cf5aea9bcc51ffbd8c683</originalsourceid><addsrcrecordid>eNptkUtLxDAUhYMoKuOs3EvBjaAdkzZN040gPkZhwI2uQ5rejBk6yZi0gv_ezMNhFLPJ434591wOQqcEjwjO-bXtu2aUYVKOyj10nGFKU4qLbH_nfISGIcxwXAxnnPFDdJTxnFQE02M0vjeyhg5CopwN8NGDVfFibNK9Q6Kh60PSmk_widOrJ-ts6moIkDSrn0Ylc6PgBB1o2QYYbvYBent8eL17Sicv4-e720mqKKZdSjSlUGW0LEhWM45LRatCMs7KRkmSMSjzQkslpeJY6UKCrGqlCqJ13XDFeD5AN2vdRV_PoVFgOy9bsfBmLv2XcNKI3xVr3sXUfYoi55hXVRS42Ah4F6cNnZiboKBtpQXXB0F4WbEiWlz2Ov-DzlzvbRwvUhXhjEQyUpdrSnkXgge9NUOwWGYklhmJZUaijPTZrv8t-5NIBK7WQIglOwW_0_QfvW9fEZye</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1891861965</pqid></control><display><type>article</type><title>Diabetes consequences in the fetus liver of the non-obese diabetic mice</title><source>NCBI_PubMed Central（免费）</source><source>Publicly Available Content Database</source><source>Springer Nature - nature.com Journals - Fully Open Access</source><creator>Aires, M B ; dos Santos, A C V ; Kubrusly, M S ; de Lima Luna, A C ; D’Albuquerque, L A C ; Maria, D A</creator><creatorcontrib>Aires, M B ; dos Santos, A C V ; Kubrusly, M S ; de Lima Luna, A C ; D’Albuquerque, L A C ; Maria, D A</creatorcontrib><description><![CDATA[DM type 1 (T1D) incidence is increasing around 3% every year and represents risks for maternal and fetal health. The objective of this study was to explore the effects of diabetes on fetus liver cells in non-obese diabetic (NOD) mice. Hyperglycemic NOD (HNOD), normoglycemic NOD (NNOD) and BALB/c females were used for mating, and the fetus livers were collected at 19.5 gestation day (gd). HNOD group had reduced fetal weight (989.5±68.32 vs 1290±57.39 mg BALB/c,
P
<0.05) at 19.5 gd and higher glycemia (516.66±28.86 mg dl
−1
,
P
<0.001) at both 0.5 gd and 19.5 gd compared to other groups. The protein expression of albumin (ALB) was significantly reduced in HNOD group (0.9±0.2 vs 3.36±0.36 NNOD
P
<0.01, vs 14.1±0.49 BALB/c
P
<0.001). Reduced gene expression of ALB (1.34±0.12 vs 5.53±0.89 NNOD and 5.23±0.71 BALB/c,
P
<0.05), Hepatic Nuclear Factor-4 alpha (HNF-4α) (0.69±0.1 vs 3.66±0.36 NNOD,
P
<0.05) and miR-122 (0.27±0,10 vs 0.88±0.15 NNOD,
P
<0.05) was present in HNOD group. No difference for alpha-Fetoprotein (AFP) and gene expression was observed. In conclusion, our findings show the impacts of T1D on the expression of ALB, AFP, HNF-4α and miR-122 in fetus liver cells by using NNOD and HNOD mice.]]></description><identifier>ISSN: 2044-4052</identifier><identifier>EISSN: 2044-4052</identifier><identifier>DOI: 10.1038/nutd.2017.7</identifier><identifier>PMID: 28319104</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/31 ; 38/90 ; 631/80/458 ; 692/163 ; Albumins - genetics ; Albumins - metabolism ; Animals ; Clinical Nutrition ; Diabetes ; Diabetes Mellitus, Type 1 - genetics ; Diabetes Mellitus, Type 1 - metabolism ; Epidemiology ; Female ; Fetus ; Gene Expression ; Hepatocyte Nuclear Factor 4 - genetics ; Hepatocyte Nuclear Factor 4 - metabolism ; Hepatocytes - metabolism ; Internal Medicine ; Liver - metabolism ; Male ; Medicine ; Medicine & Public Health ; Metabolic Diseases ; Mice, Inbred NOD ; MicroRNAs - genetics ; MicroRNAs - metabolism ; Short Communication</subject><ispartof>Nutrition & diabetes, 2017-03, Vol.7 (3), p.e257-e257</ispartof><rights>The Author(s) 2017</rights><rights>Copyright Nature Publishing Group Mar 2017</rights><rights>Copyright © 2017 The Author(s) 2017 The Author(s)</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c404t-1f44e9247512b6807c495a6867dca126e735facaac80cf5aea9bcc51ffbd8c683</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/1891861965/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/1891861965?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,37013,44590,53791,53793,74998</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28319104$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Aires, M B</creatorcontrib><creatorcontrib>dos Santos, A C V</creatorcontrib><creatorcontrib>Kubrusly, M S</creatorcontrib><creatorcontrib>de Lima Luna, A C</creatorcontrib><creatorcontrib>D’Albuquerque, L A C</creatorcontrib><creatorcontrib>Maria, D A</creatorcontrib><title>Diabetes consequences in the fetus liver of the non-obese diabetic mice</title><title>Nutrition & diabetes</title><addtitle>Nutr & Diabetes</addtitle><addtitle>Nutr Diabetes</addtitle><description><![CDATA[DM type 1 (T1D) incidence is increasing around 3% every year and represents risks for maternal and fetal health. The objective of this study was to explore the effects of diabetes on fetus liver cells in non-obese diabetic (NOD) mice. Hyperglycemic NOD (HNOD), normoglycemic NOD (NNOD) and BALB/c females were used for mating, and the fetus livers were collected at 19.5 gestation day (gd). HNOD group had reduced fetal weight (989.5±68.32 vs 1290±57.39 mg BALB/c,
P
<0.05) at 19.5 gd and higher glycemia (516.66±28.86 mg dl
−1
,
P
<0.001) at both 0.5 gd and 19.5 gd compared to other groups. The protein expression of albumin (ALB) was significantly reduced in HNOD group (0.9±0.2 vs 3.36±0.36 NNOD
P
<0.01, vs 14.1±0.49 BALB/c
P
<0.001). Reduced gene expression of ALB (1.34±0.12 vs 5.53±0.89 NNOD and 5.23±0.71 BALB/c,
P
<0.05), Hepatic Nuclear Factor-4 alpha (HNF-4α) (0.69±0.1 vs 3.66±0.36 NNOD,
P
<0.05) and miR-122 (0.27±0,10 vs 0.88±0.15 NNOD,
P
<0.05) was present in HNOD group. No difference for alpha-Fetoprotein (AFP) and gene expression was observed. In conclusion, our findings show the impacts of T1D on the expression of ALB, AFP, HNF-4α and miR-122 in fetus liver cells by using NNOD and HNOD mice.]]></description><subject>13/31</subject><subject>38/90</subject><subject>631/80/458</subject><subject>692/163</subject><subject>Albumins - genetics</subject><subject>Albumins - metabolism</subject><subject>Animals</subject><subject>Clinical Nutrition</subject><subject>Diabetes</subject><subject>Diabetes Mellitus, Type 1 - genetics</subject><subject>Diabetes Mellitus, Type 1 - metabolism</subject><subject>Epidemiology</subject><subject>Female</subject><subject>Fetus</subject><subject>Gene Expression</subject><subject>Hepatocyte Nuclear Factor 4 - genetics</subject><subject>Hepatocyte Nuclear Factor 4 - metabolism</subject><subject>Hepatocytes - metabolism</subject><subject>Internal Medicine</subject><subject>Liver - metabolism</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Metabolic Diseases</subject><subject>Mice, Inbred NOD</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>Short Communication</subject><issn>2044-4052</issn><issn>2044-4052</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><recordid>eNptkUtLxDAUhYMoKuOs3EvBjaAdkzZN040gPkZhwI2uQ5rejBk6yZi0gv_ezMNhFLPJ434591wOQqcEjwjO-bXtu2aUYVKOyj10nGFKU4qLbH_nfISGIcxwXAxnnPFDdJTxnFQE02M0vjeyhg5CopwN8NGDVfFibNK9Q6Kh60PSmk_widOrJ-ts6moIkDSrn0Ylc6PgBB1o2QYYbvYBent8eL17Sicv4-e720mqKKZdSjSlUGW0LEhWM45LRatCMs7KRkmSMSjzQkslpeJY6UKCrGqlCqJ13XDFeD5AN2vdRV_PoVFgOy9bsfBmLv2XcNKI3xVr3sXUfYoi55hXVRS42Ah4F6cNnZiboKBtpQXXB0F4WbEiWlz2Ov-DzlzvbRwvUhXhjEQyUpdrSnkXgge9NUOwWGYklhmJZUaijPTZrv8t-5NIBK7WQIglOwW_0_QfvW9fEZye</recordid><startdate>20170320</startdate><enddate>20170320</enddate><creator>Aires, M B</creator><creator>dos Santos, A C V</creator><creator>Kubrusly, M S</creator><creator>de Lima Luna, A C</creator><creator>D’Albuquerque, L A C</creator><creator>Maria, D A</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>C6C</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>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</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>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20170320</creationdate><title>Diabetes consequences in the fetus liver of the non-obese diabetic mice</title><author>Aires, M B ; dos Santos, A C V ; Kubrusly, M S ; de Lima Luna, A C ; D’Albuquerque, L A C ; Maria, D A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c404t-1f44e9247512b6807c495a6867dca126e735facaac80cf5aea9bcc51ffbd8c683</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>13/31</topic><topic>38/90</topic><topic>631/80/458</topic><topic>692/163</topic><topic>Albumins - genetics</topic><topic>Albumins - metabolism</topic><topic>Animals</topic><topic>Clinical Nutrition</topic><topic>Diabetes</topic><topic>Diabetes Mellitus, Type 1 - genetics</topic><topic>Diabetes Mellitus, Type 1 - metabolism</topic><topic>Epidemiology</topic><topic>Female</topic><topic>Fetus</topic><topic>Gene Expression</topic><topic>Hepatocyte Nuclear Factor 4 - genetics</topic><topic>Hepatocyte Nuclear Factor 4 - metabolism</topic><topic>Hepatocytes - metabolism</topic><topic>Internal Medicine</topic><topic>Liver - metabolism</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Metabolic Diseases</topic><topic>Mice, Inbred NOD</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>Short Communication</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Aires, M B</creatorcontrib><creatorcontrib>dos Santos, A C V</creatorcontrib><creatorcontrib>Kubrusly, M S</creatorcontrib><creatorcontrib>de Lima Luna, A C</creatorcontrib><creatorcontrib>D’Albuquerque, L A C</creatorcontrib><creatorcontrib>Maria, D A</creatorcontrib><collection>Springer_OA刊</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>ProQuest_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>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central</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 Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Nutrition & diabetes</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Aires, M B</au><au>dos Santos, A C V</au><au>Kubrusly, M S</au><au>de Lima Luna, A C</au><au>D’Albuquerque, L A C</au><au>Maria, D A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Diabetes consequences in the fetus liver of the non-obese diabetic mice</atitle><jtitle>Nutrition & diabetes</jtitle><stitle>Nutr & Diabetes</stitle><addtitle>Nutr Diabetes</addtitle><date>2017-03-20</date><risdate>2017</risdate><volume>7</volume><issue>3</issue><spage>e257</spage><epage>e257</epage><pages>e257-e257</pages><issn>2044-4052</issn><eissn>2044-4052</eissn><abstract><![CDATA[DM type 1 (T1D) incidence is increasing around 3% every year and represents risks for maternal and fetal health. The objective of this study was to explore the effects of diabetes on fetus liver cells in non-obese diabetic (NOD) mice. Hyperglycemic NOD (HNOD), normoglycemic NOD (NNOD) and BALB/c females were used for mating, and the fetus livers were collected at 19.5 gestation day (gd). HNOD group had reduced fetal weight (989.5±68.32 vs 1290±57.39 mg BALB/c,
P
<0.05) at 19.5 gd and higher glycemia (516.66±28.86 mg dl
−1
,
P
<0.001) at both 0.5 gd and 19.5 gd compared to other groups. The protein expression of albumin (ALB) was significantly reduced in HNOD group (0.9±0.2 vs 3.36±0.36 NNOD
P
<0.01, vs 14.1±0.49 BALB/c
P
<0.001). Reduced gene expression of ALB (1.34±0.12 vs 5.53±0.89 NNOD and 5.23±0.71 BALB/c,
P
<0.05), Hepatic Nuclear Factor-4 alpha (HNF-4α) (0.69±0.1 vs 3.66±0.36 NNOD,
P
<0.05) and miR-122 (0.27±0,10 vs 0.88±0.15 NNOD,
P
<0.05) was present in HNOD group. No difference for alpha-Fetoprotein (AFP) and gene expression was observed. In conclusion, our findings show the impacts of T1D on the expression of ALB, AFP, HNF-4α and miR-122 in fetus liver cells by using NNOD and HNOD mice.]]></abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>28319104</pmid><doi>10.1038/nutd.2017.7</doi><oa>free_for_read</oa></addata></record> |
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| subjects | 13/31 38/90 631/80/458 692/163 Albumins - genetics Albumins - metabolism Animals Clinical Nutrition Diabetes Diabetes Mellitus, Type 1 - genetics Diabetes Mellitus, Type 1 - metabolism Epidemiology Female Fetus Gene Expression Hepatocyte Nuclear Factor 4 - genetics Hepatocyte Nuclear Factor 4 - metabolism Hepatocytes - metabolism Internal Medicine Liver - metabolism Male Medicine Medicine & Public Health Metabolic Diseases Mice, Inbred NOD MicroRNAs - genetics MicroRNAs - metabolism Short Communication |
| title | Diabetes consequences in the fetus liver of the non-obese diabetic mice |
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