dc.date.accessioned | 2022-02-04T18:52:26Z | |
dc.date.available | 2022-02-04T18:52:26Z | |
dc.date.created | 2022-01-11T13:13:04Z | |
dc.date.issued | 2021 | |
dc.identifier.citation | Sletner, Line Moen, Aina Elisabeth Fossum Yajnik, Chittaranjan S Lekanova, Nadezhda Sommer, Christine Birkeland, Kåre Inge Jenum, Anne Karen Böttcher, Yvonne . Maternal Glucose and LDL-Cholesterol Levels Are Related to Placental Leptin Gene Methylation, and, Together With Nutritional Factors, Largely Explain a Higher Methylation Level Among Ethnic South Asians. Frontiers in Endocrinology. 2021 | |
dc.identifier.uri | http://hdl.handle.net/10852/90507 | |
dc.description.abstract | Background Leptin, mainly secreted by fat cells, plays a core role in the regulation of appetite and body weight, and has been proposed as a mediator of metabolic programming. During pregnancy leptin is also secreted by the placenta, as well as being a key regulatory cytokine for the development, homeostatic regulation and nutrient transport within the placenta. South Asians have a high burden of type 2 diabetes, partly attributed to a “thin-fat-phenotype”. Objective Our aim was to investigate how maternal ethnicity, adiposity and glucose- and lipid/cholesterol levels in pregnancy are related to placental leptin gene ( LEP ) DNA methylation. Methods We performed DNA methylation analyses of 13 placental LEP CpG sites in 40 ethnic Europeans and 40 ethnic South Asians participating in the STORK-Groruddalen cohort. Results South Asian ethnicity and gestational diabetes (GDM) were associated with higher placental LEP methylation. The largest ethnic difference was found for CpG11 [5.8% (95% CI: 2.4, 9.2), p<0.001], and the strongest associations with GDM was seen for CpG5 [5.2% (1.4, 9.0), p=0.008]. Higher maternal LDL-cholesterol was associated with lower placental LEP methylation, in particular for CpG11 [-3.6% (-5.5, -1.4) per one mmol/L increase in LDL, p<0.001]. After adjustments, including for nutritional factors involved in the one-carbon-metabolism cycle (vitamin D, B12 and folate levels), ethnic differences in placental LEP methylation were strongly attenuated, while associations with glucose and LDL-cholesterol persisted. Conclusions Maternal glucose and lipid metabolism is related to placental LEP methylation, whilst metabolic and nutritional factors largely explain a higher methylation level among ethnic South Asians. | |
dc.language | EN | |
dc.rights | Attribution 4.0 International | |
dc.rights.uri | https://creativecommons.org/licenses/by/4.0/ | |
dc.title | Maternal Glucose and LDL-Cholesterol Levels Are Related to Placental Leptin Gene Methylation, and, Together With Nutritional Factors, Largely Explain a Higher Methylation Level Among Ethnic South Asians | |
dc.type | Journal article | |
dc.creator.author | Sletner, Line | |
dc.creator.author | Moen, Aina Elisabeth Fossum | |
dc.creator.author | Yajnik, Chittaranjan S | |
dc.creator.author | Lekanova, Nadezhda | |
dc.creator.author | Sommer, Christine | |
dc.creator.author | Birkeland, Kåre Inge | |
dc.creator.author | Jenum, Anne Karen | |
dc.creator.author | Böttcher, Yvonne | |
cristin.unitcode | 185,53,82,0 | |
cristin.unitname | Klinikk for indremedisin og lab fag | |
cristin.ispublished | true | |
cristin.fulltext | original | |
cristin.qualitycode | 1 | |
dc.identifier.cristin | 1978356 | |
dc.identifier.bibliographiccitation | info:ofi/fmt:kev:mtx:ctx&ctx_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.jtitle=Frontiers in Endocrinology&rft.volume=&rft.spage=&rft.date=2021 | |
dc.identifier.jtitle | Frontiers in Endocrinology | |
dc.identifier.volume | 12 | |
dc.identifier.doi | https://doi.org/10.3389/fendo.2021.809916 | |
dc.identifier.urn | URN:NBN:no-93123 | |
dc.type.document | Tidsskriftartikkel | |
dc.type.peerreviewed | Peer reviewed | |
dc.source.issn | 1664-2392 | |
dc.identifier.fulltext | Fulltext https://www.duo.uio.no/bitstream/handle/10852/90507/1/fendo-12-809916.pdf | |
dc.type.version | PublishedVersion | |
cristin.articleid | 89916 | |
dc.relation.project | HSØ/2017-063 | |