The effect of pre-existing maternal obesity and diabetes on placental mitochondrial content and electron transport chain activity
Abstract Introduction Mitochondria dysfunction has been extensively implicated in the progression of these metabolic disorders, their role in placental tissue of diabetic and/or obese pregnant women is yet to be investigated. The aim of this study was to determine the effect of pre-existing type 1 a...
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| Veröffentlicht in: | Placenta (Eastbourne) 2014-09, Vol.35 (9), p.673-683 |
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| description | Abstract Introduction Mitochondria dysfunction has been extensively implicated in the progression of these metabolic disorders, their role in placental tissue of diabetic and/or obese pregnant women is yet to be investigated. The aim of this study was to determine the effect of pre-existing type 1 and type 2 diabetes mellitus (DM), and pre-existing maternal obesity on placental mitochondrial function as assessed by mitochondrial content, electron transport chain (ETC) complex activities and oxidative stress. Methods Human placenta was obtained at the time of term Caesarean section from (i) non-obese ( n = 19) and obese ( n = 23) normal glucose tolerant (NGT) pregnant women; (ii) women with type 1 DM ( n = 14) and BMI-matched NGT women ( n = 14); and (iii) women with type 2 DM ( n = 11) and BMI-matched NGT women ( n = 11). The following endpoints were assessed: placental mitochondrial content by citrate synthase activity and mitochondrial DNA (mtDNA content); mitochondrial respiratory chain activity (complexes I, II, II & III, III and IV), and mitochondrial ROS (as assessed by mitochondrial hydrogen peroxide (H2 O2 ) levels). Results When compared to placenta from NGT non-obese women, there was significantly lower mitochondrial DNA (mtDNA) content and electron transport chain complex I activity, and significantly higher mitochondrial H2 O2 levels in placenta from NGT obese women ( P |
| doi_str_mv | 10.1016/j.placenta.2014.06.368 |
| format | Article |
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The aim of this study was to determine the effect of pre-existing type 1 and type 2 diabetes mellitus (DM), and pre-existing maternal obesity on placental mitochondrial function as assessed by mitochondrial content, electron transport chain (ETC) complex activities and oxidative stress. Methods Human placenta was obtained at the time of term Caesarean section from (i) non-obese ( n = 19) and obese ( n = 23) normal glucose tolerant (NGT) pregnant women; (ii) women with type 1 DM ( n = 14) and BMI-matched NGT women ( n = 14); and (iii) women with type 2 DM ( n = 11) and BMI-matched NGT women ( n = 11). The following endpoints were assessed: placental mitochondrial content by citrate synthase activity and mitochondrial DNA (mtDNA content); mitochondrial respiratory chain activity (complexes I, II, II & III, III and IV), and mitochondrial ROS (as assessed by mitochondrial hydrogen peroxide (H2 O2 ) levels). Results When compared to placenta from NGT non-obese women, there was significantly lower mitochondrial DNA (mtDNA) content and electron transport chain complex I activity, and significantly higher mitochondrial H2 O2 levels in placenta from NGT obese women ( P < 0.05). Placental tissue from type 1 DM women showed significant reductions in ETC complex I, II & III, and III activity and increased H2 O2 levels when compared to BMI-matched NGT women ( P < 0.05). Type 2 DM women only exhibited significantly reduced ETC complex II & III activity when compared to BMI-matched NGT women ( P < 0.05). Discussion and conclusions Women with pre-existing obesity or diabetes have decreased placental mitochondrial respiratory chain enzyme activities which may have detrimental consequences on placental function and therefore fetal growth and development.]]></description><identifier>ISSN: 0143-4004</identifier><identifier>EISSN: 1532-3102</identifier><identifier>DOI: 10.1016/j.placenta.2014.06.368</identifier><identifier>PMID: 25002362</identifier><identifier>CODEN: PLACDF</identifier><language>eng</language><publisher>Kidlington: Elsevier Ltd</publisher><subject>Adult ; Biological and medical sciences ; Case-Control Studies ; Cell Respiration ; Diabetes Mellitus, Type 1 - metabolism ; Diabetes Mellitus, Type 2 - metabolism ; Electron Transport ; Embryology: invertebrates and vertebrates. Teratology ; Female ; Fundamental and applied biological sciences. Psychology ; Humans ; Internal Medicine ; Mitochondria ; Mitochondria - metabolism ; Obesity - metabolism ; Obstetrics and Gynecology ; Placenta ; Placenta - metabolism ; Pre-existing maternal obesity ; Pregnancy ; Pregnancy in Diabetics - metabolism ; Reactive Oxygen Species - metabolism ; Type 1 DM ; Type 2 DM</subject><ispartof>Placenta (Eastbourne), 2014-09, Vol.35 (9), p.673-683</ispartof><rights>Elsevier Ltd</rights><rights>2014 Elsevier Ltd</rights><rights>2015 INIST-CNRS</rights><rights>Copyright © 2014 Elsevier Ltd. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c453t-58acbc0ff47d404157a5235c875183ae7ff9a4c462464c55a7f25354d9d46abc3</citedby><cites>FETCH-LOGICAL-c453t-58acbc0ff47d404157a5235c875183ae7ff9a4c462464c55a7f25354d9d46abc3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0143400414005943$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65534</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=28740764$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25002362$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hastie, R</creatorcontrib><creatorcontrib>Lappas, M</creatorcontrib><title>The effect of pre-existing maternal obesity and diabetes on placental mitochondrial content and electron transport chain activity</title><title>Placenta (Eastbourne)</title><addtitle>Placenta</addtitle><description><![CDATA[Abstract Introduction Mitochondria dysfunction has been extensively implicated in the progression of these metabolic disorders, their role in placental tissue of diabetic and/or obese pregnant women is yet to be investigated. The aim of this study was to determine the effect of pre-existing type 1 and type 2 diabetes mellitus (DM), and pre-existing maternal obesity on placental mitochondrial function as assessed by mitochondrial content, electron transport chain (ETC) complex activities and oxidative stress. Methods Human placenta was obtained at the time of term Caesarean section from (i) non-obese ( n = 19) and obese ( n = 23) normal glucose tolerant (NGT) pregnant women; (ii) women with type 1 DM ( n = 14) and BMI-matched NGT women ( n = 14); and (iii) women with type 2 DM ( n = 11) and BMI-matched NGT women ( n = 11). The following endpoints were assessed: placental mitochondrial content by citrate synthase activity and mitochondrial DNA (mtDNA content); mitochondrial respiratory chain activity (complexes I, II, II & III, III and IV), and mitochondrial ROS (as assessed by mitochondrial hydrogen peroxide (H2 O2 ) levels). Results When compared to placenta from NGT non-obese women, there was significantly lower mitochondrial DNA (mtDNA) content and electron transport chain complex I activity, and significantly higher mitochondrial H2 O2 levels in placenta from NGT obese women ( P < 0.05). Placental tissue from type 1 DM women showed significant reductions in ETC complex I, II & III, and III activity and increased H2 O2 levels when compared to BMI-matched NGT women ( P < 0.05). Type 2 DM women only exhibited significantly reduced ETC complex II & III activity when compared to BMI-matched NGT women ( P < 0.05). Discussion and conclusions Women with pre-existing obesity or diabetes have decreased placental mitochondrial respiratory chain enzyme activities which may have detrimental consequences on placental function and therefore fetal growth and development.]]></description><subject>Adult</subject><subject>Biological and medical sciences</subject><subject>Case-Control Studies</subject><subject>Cell Respiration</subject><subject>Diabetes Mellitus, Type 1 - metabolism</subject><subject>Diabetes Mellitus, Type 2 - metabolism</subject><subject>Electron Transport</subject><subject>Embryology: invertebrates and vertebrates. Teratology</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Humans</subject><subject>Internal Medicine</subject><subject>Mitochondria</subject><subject>Mitochondria - metabolism</subject><subject>Obesity - metabolism</subject><subject>Obstetrics and Gynecology</subject><subject>Placenta</subject><subject>Placenta - metabolism</subject><subject>Pre-existing maternal obesity</subject><subject>Pregnancy</subject><subject>Pregnancy in Diabetics - metabolism</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Type 1 DM</subject><subject>Type 2 DM</subject><issn>0143-4004</issn><issn>1532-3102</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkk2PFCEQhonRuLOrf2HDxcRLt3x3z8VoNuqabOLB9UxounAYu2EEZuMc_efSzowmXrxAgKfeqnophK4paSmh6tW23U3GQiimZYSKlqiWq_4RWlHJWcMpYY_Rqj7wRhAiLtBlzltCyFpQ9hRdMEkI44qt0M_7DWBwDmzB0eFdggZ--Fx8-IpnUyAFM-E4QPblgE0Y8ejNAAUyjgGfS5jw7Eu0mxjG5OvJxlDq_W8epiqdKlySCXkXU8F2Y3zAxhb_UFWfoSfOTBmen_Yr9OX9u_ub2-bu04ePN2_vGiskL43sjR0scU50oyCCys5IxqXtO0l7bqBzbm2EFYoJJayUpnNMcinG9SiUGSy_Qi-PursUv-8hFz37bGGaTIC4z5pKqVgvmGAVVUfUpphzAqd3yc8mHTQlerFfb_W5d73Yr4nS1f4aeH3KsR9mGP-Enf2uwIsTYLI1k6ueWJ__cn0nSKdE5d4cOaiOPHhIOlsPwcLoU_VTj9H_v5bX_0jYyQdfs36DA-Rt3C9_W_vWmWmiPy_DsswKrYtcC85_ARP7vck</recordid><startdate>20140901</startdate><enddate>20140901</enddate><creator>Hastie, R</creator><creator>Lappas, M</creator><general>Elsevier Ltd</general><general>Elsevier</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>7X8</scope></search><sort><creationdate>20140901</creationdate><title>The effect of pre-existing maternal obesity and diabetes on placental mitochondrial content and electron transport chain activity</title><author>Hastie, R ; Lappas, M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c453t-58acbc0ff47d404157a5235c875183ae7ff9a4c462464c55a7f25354d9d46abc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Adult</topic><topic>Biological and medical sciences</topic><topic>Case-Control Studies</topic><topic>Cell Respiration</topic><topic>Diabetes Mellitus, Type 1 - metabolism</topic><topic>Diabetes Mellitus, Type 2 - metabolism</topic><topic>Electron Transport</topic><topic>Embryology: invertebrates and vertebrates. Teratology</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Humans</topic><topic>Internal Medicine</topic><topic>Mitochondria</topic><topic>Mitochondria - metabolism</topic><topic>Obesity - metabolism</topic><topic>Obstetrics and Gynecology</topic><topic>Placenta</topic><topic>Placenta - metabolism</topic><topic>Pre-existing maternal obesity</topic><topic>Pregnancy</topic><topic>Pregnancy in Diabetics - metabolism</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Type 1 DM</topic><topic>Type 2 DM</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hastie, R</creatorcontrib><creatorcontrib>Lappas, M</creatorcontrib><collection>Pascal-Francis</collection><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><jtitle>Placenta (Eastbourne)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hastie, R</au><au>Lappas, M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The effect of pre-existing maternal obesity and diabetes on placental mitochondrial content and electron transport chain activity</atitle><jtitle>Placenta (Eastbourne)</jtitle><addtitle>Placenta</addtitle><date>2014-09-01</date><risdate>2014</risdate><volume>35</volume><issue>9</issue><spage>673</spage><epage>683</epage><pages>673-683</pages><issn>0143-4004</issn><eissn>1532-3102</eissn><coden>PLACDF</coden><abstract><![CDATA[Abstract Introduction Mitochondria dysfunction has been extensively implicated in the progression of these metabolic disorders, their role in placental tissue of diabetic and/or obese pregnant women is yet to be investigated. The aim of this study was to determine the effect of pre-existing type 1 and type 2 diabetes mellitus (DM), and pre-existing maternal obesity on placental mitochondrial function as assessed by mitochondrial content, electron transport chain (ETC) complex activities and oxidative stress. Methods Human placenta was obtained at the time of term Caesarean section from (i) non-obese ( n = 19) and obese ( n = 23) normal glucose tolerant (NGT) pregnant women; (ii) women with type 1 DM ( n = 14) and BMI-matched NGT women ( n = 14); and (iii) women with type 2 DM ( n = 11) and BMI-matched NGT women ( n = 11). The following endpoints were assessed: placental mitochondrial content by citrate synthase activity and mitochondrial DNA (mtDNA content); mitochondrial respiratory chain activity (complexes I, II, II & III, III and IV), and mitochondrial ROS (as assessed by mitochondrial hydrogen peroxide (H2 O2 ) levels). Results When compared to placenta from NGT non-obese women, there was significantly lower mitochondrial DNA (mtDNA) content and electron transport chain complex I activity, and significantly higher mitochondrial H2 O2 levels in placenta from NGT obese women ( P < 0.05). Placental tissue from type 1 DM women showed significant reductions in ETC complex I, II & III, and III activity and increased H2 O2 levels when compared to BMI-matched NGT women ( P < 0.05). Type 2 DM women only exhibited significantly reduced ETC complex II & III activity when compared to BMI-matched NGT women ( P < 0.05). Discussion and conclusions Women with pre-existing obesity or diabetes have decreased placental mitochondrial respiratory chain enzyme activities which may have detrimental consequences on placental function and therefore fetal growth and development.]]></abstract><cop>Kidlington</cop><pub>Elsevier Ltd</pub><pmid>25002362</pmid><doi>10.1016/j.placenta.2014.06.368</doi><tpages>11</tpages></addata></record> |
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| subjects | Adult Biological and medical sciences Case-Control Studies Cell Respiration Diabetes Mellitus, Type 1 - metabolism Diabetes Mellitus, Type 2 - metabolism Electron Transport Embryology: invertebrates and vertebrates. Teratology Female Fundamental and applied biological sciences. Psychology Humans Internal Medicine Mitochondria Mitochondria - metabolism Obesity - metabolism Obstetrics and Gynecology Placenta Placenta - metabolism Pre-existing maternal obesity Pregnancy Pregnancy in Diabetics - metabolism Reactive Oxygen Species - metabolism Type 1 DM Type 2 DM |
| title | The effect of pre-existing maternal obesity and diabetes on placental mitochondrial content and electron transport chain activity |
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