The expression of genes involved in NF-κB activation in peripheral blood mononuclear cells of patients with gestational diabetes

ObjectiveIn patients with obesity and type 2 diabetes, the changes in insulin resistance are associated with the changes in expression of genes involved in nuclear factor-κB (NF-κB) activation in peripheral blood mononuclear cells (PBMCs). As such studies have never been carried out in patients with...

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Veröffentlicht in:European journal of endocrinology 2013-03, Vol.168 (3), p.419-427
Hauptverfasser: Kuzmicki, Mariusz, Telejko, Beata, Wawrusiewicz-Kurylonek, Natalia, Lipinska, Danuta, Pliszka, Justyna, Wilk, Julisz, Zielinska, Anna, Skibicka, Justyna, Szamatowicz, Jacek, Kretowski, Adam, Gorska, M
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container_end_page 427
container_issue 3
container_start_page 419
container_title European journal of endocrinology
container_volume 168
creator Kuzmicki, Mariusz
Telejko, Beata
Wawrusiewicz-Kurylonek, Natalia
Lipinska, Danuta
Pliszka, Justyna
Wilk, Julisz
Zielinska, Anna
Skibicka, Justyna
Szamatowicz, Jacek
Kretowski, Adam
Gorska, M
description ObjectiveIn patients with obesity and type 2 diabetes, the changes in insulin resistance are associated with the changes in expression of genes involved in nuclear factor-κB (NF-κB) activation in peripheral blood mononuclear cells (PBMCs). As such studies have never been carried out in patients with gestational diabetes (GDM), in this study, we evaluated the expression of genes involved in NF-κB activation and related to glucose metabolism in PBMCs obtained from pregnant women with GDM and normal glucose tolerance (NGT).Design and methodsRT-PCR was performed in 60 pregnant women divided into three groups: GDM at the 1st visit, i.e. in the 24th–28th weeks of gestation (GDM1), NGT at the first visit and GDM in the 29th–32nd weeks (GDM2), and NGT at both visits. The tests were repeated 3 months postpartum.ResultsThe GDM1 group had significantly higher TLR2 (P=0.024), TLR4 (P=0.037), STAT1 (P=0.027), and CX3CL1 (P=0.017) mRNA expression, whereas the GDM2 group showed markedly lower TNFRSF1A (P=0.042), PPARG (P=0.018), STAT3 (P=0.013), and CX3CL1 (P=0.038) mRNA expression in comparison with the NGT group. The women with NGT at the 1st visit who later developed GDM had significantly higher fasting glucose (P=0.01), HOMA-IR (P=0.004), and TLR2 mRNA expression (P=0.04), as well as lower ISSI2 (P=0.01) and disposition indices, DI30 (P=0.03) and DI120 (P=0.01), than had the women who remained normoglycemic.ConclusionsOur results suggest that elevated TLR2 expression, as well as higher fasting glucose and lower compensation for increased insulin resistance, may represent early metabolic disturbances in the development of GDM.
doi_str_mv 10.1530/EJE-12-0654
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As such studies have never been carried out in patients with gestational diabetes (GDM), in this study, we evaluated the expression of genes involved in NF-κB activation and related to glucose metabolism in PBMCs obtained from pregnant women with GDM and normal glucose tolerance (NGT).Design and methodsRT-PCR was performed in 60 pregnant women divided into three groups: GDM at the 1st visit, i.e. in the 24th–28th weeks of gestation (GDM1), NGT at the first visit and GDM in the 29th–32nd weeks (GDM2), and NGT at both visits. The tests were repeated 3 months postpartum.ResultsThe GDM1 group had significantly higher TLR2 (P=0.024), TLR4 (P=0.037), STAT1 (P=0.027), and CX3CL1 (P=0.017) mRNA expression, whereas the GDM2 group showed markedly lower TNFRSF1A (P=0.042), PPARG (P=0.018), STAT3 (P=0.013), and CX3CL1 (P=0.038) mRNA expression in comparison with the NGT group. The women with NGT at the 1st visit who later developed GDM had significantly higher fasting glucose (P=0.01), HOMA-IR (P=0.004), and TLR2 mRNA expression (P=0.04), as well as lower ISSI2 (P=0.01) and disposition indices, DI30 (P=0.03) and DI120 (P=0.01), than had the women who remained normoglycemic.ConclusionsOur results suggest that elevated TLR2 expression, as well as higher fasting glucose and lower compensation for increased insulin resistance, may represent early metabolic disturbances in the development of GDM.</description><identifier>ISSN: 0804-4643</identifier><identifier>EISSN: 1479-683X</identifier><identifier>DOI: 10.1530/EJE-12-0654</identifier><identifier>PMID: 23230212</identifier><language>eng</language><publisher>Bristol: BioScientifica</publisher><subject>Adult ; Biological and medical sciences ; Blood Glucose - analysis ; Chemokine CX3CL1 - genetics ; Chemokine CX3CL1 - metabolism ; Clinical Study ; Diabetes, Gestational - blood ; Diabetes, Gestational - diagnosis ; Diabetes, Gestational - metabolism ; Early Diagnosis ; Endocrinopathies ; Female ; Fundamental and applied biological sciences. Psychology ; Gene Expression Regulation ; Humans ; Insulin Resistance ; Leukocytes, Mononuclear - metabolism ; Medical sciences ; NF-kappa B p50 Subunit - blood ; NF-kappa B p50 Subunit - metabolism ; PPAR gamma - genetics ; PPAR gamma - metabolism ; Pregnancy ; Pregnancy Trimester, Second ; Pregnancy Trimester, Third ; Receptors, Tumor Necrosis Factor, Type I - genetics ; Receptors, Tumor Necrosis Factor, Type I - metabolism ; RNA, Messenger - metabolism ; STAT Transcription Factors - genetics ; STAT Transcription Factors - metabolism ; Toll-Like Receptor 2 - genetics ; Toll-Like Receptor 2 - metabolism ; Toll-Like Receptor 4 - genetics ; Toll-Like Receptor 4 - metabolism ; Vertebrates: endocrinology</subject><ispartof>European journal of endocrinology, 2013-03, Vol.168 (3), p.419-427</ispartof><rights>2013 European Society of Endocrinology</rights><rights>2014 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b398t-d5a907c6b63f5d5e1ef22a020ac181821a0904d8877eb5402b66ccc52c8f74913</citedby><cites>FETCH-LOGICAL-b398t-d5a907c6b63f5d5e1ef22a020ac181821a0904d8877eb5402b66ccc52c8f74913</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&amp;idt=27158717$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23230212$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kuzmicki, Mariusz</creatorcontrib><creatorcontrib>Telejko, Beata</creatorcontrib><creatorcontrib>Wawrusiewicz-Kurylonek, Natalia</creatorcontrib><creatorcontrib>Lipinska, Danuta</creatorcontrib><creatorcontrib>Pliszka, Justyna</creatorcontrib><creatorcontrib>Wilk, Julisz</creatorcontrib><creatorcontrib>Zielinska, Anna</creatorcontrib><creatorcontrib>Skibicka, Justyna</creatorcontrib><creatorcontrib>Szamatowicz, Jacek</creatorcontrib><creatorcontrib>Kretowski, Adam</creatorcontrib><creatorcontrib>Gorska, M</creatorcontrib><title>The expression of genes involved in NF-κB activation in peripheral blood mononuclear cells of patients with gestational diabetes</title><title>European journal of endocrinology</title><addtitle>Eur J Endocrinol</addtitle><description>ObjectiveIn patients with obesity and type 2 diabetes, the changes in insulin resistance are associated with the changes in expression of genes involved in nuclear factor-κB (NF-κB) activation in peripheral blood mononuclear cells (PBMCs). As such studies have never been carried out in patients with gestational diabetes (GDM), in this study, we evaluated the expression of genes involved in NF-κB activation and related to glucose metabolism in PBMCs obtained from pregnant women with GDM and normal glucose tolerance (NGT).Design and methodsRT-PCR was performed in 60 pregnant women divided into three groups: GDM at the 1st visit, i.e. in the 24th–28th weeks of gestation (GDM1), NGT at the first visit and GDM in the 29th–32nd weeks (GDM2), and NGT at both visits. The tests were repeated 3 months postpartum.ResultsThe GDM1 group had significantly higher TLR2 (P=0.024), TLR4 (P=0.037), STAT1 (P=0.027), and CX3CL1 (P=0.017) mRNA expression, whereas the GDM2 group showed markedly lower TNFRSF1A (P=0.042), PPARG (P=0.018), STAT3 (P=0.013), and CX3CL1 (P=0.038) mRNA expression in comparison with the NGT group. The women with NGT at the 1st visit who later developed GDM had significantly higher fasting glucose (P=0.01), HOMA-IR (P=0.004), and TLR2 mRNA expression (P=0.04), as well as lower ISSI2 (P=0.01) and disposition indices, DI30 (P=0.03) and DI120 (P=0.01), than had the women who remained normoglycemic.ConclusionsOur results suggest that elevated TLR2 expression, as well as higher fasting glucose and lower compensation for increased insulin resistance, may represent early metabolic disturbances in the development of GDM.</description><subject>Adult</subject><subject>Biological and medical sciences</subject><subject>Blood Glucose - analysis</subject><subject>Chemokine CX3CL1 - genetics</subject><subject>Chemokine CX3CL1 - metabolism</subject><subject>Clinical Study</subject><subject>Diabetes, Gestational - blood</subject><subject>Diabetes, Gestational - diagnosis</subject><subject>Diabetes, Gestational - metabolism</subject><subject>Early Diagnosis</subject><subject>Endocrinopathies</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene Expression Regulation</subject><subject>Humans</subject><subject>Insulin Resistance</subject><subject>Leukocytes, Mononuclear - metabolism</subject><subject>Medical sciences</subject><subject>NF-kappa B p50 Subunit - blood</subject><subject>NF-kappa B p50 Subunit - metabolism</subject><subject>PPAR gamma - genetics</subject><subject>PPAR gamma - metabolism</subject><subject>Pregnancy</subject><subject>Pregnancy Trimester, Second</subject><subject>Pregnancy Trimester, Third</subject><subject>Receptors, Tumor Necrosis Factor, Type I - genetics</subject><subject>Receptors, Tumor Necrosis Factor, Type I - metabolism</subject><subject>RNA, Messenger - metabolism</subject><subject>STAT Transcription Factors - genetics</subject><subject>STAT Transcription Factors - metabolism</subject><subject>Toll-Like Receptor 2 - genetics</subject><subject>Toll-Like Receptor 2 - metabolism</subject><subject>Toll-Like Receptor 4 - genetics</subject><subject>Toll-Like Receptor 4 - metabolism</subject><subject>Vertebrates: endocrinology</subject><issn>0804-4643</issn><issn>1479-683X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp90MFu1DAQBmALUdGlcOKOfEFCQike24mdI622QFXBpUjcIseZsEbZOHiyCz3yWjwEz4TDLnDj5JH1-ffoZ-wJiHMolXi5vl4XIAtRlfoeW4E2dVFZ9fE-WwkrdKErrU7ZQ6LPQkCexQN2KpVUQoJcse-3G-T4bUpIFOLIY88_4YjEw7iPwx67PPB3V8XPHxfc-Tns3bywfDlhCtMGkxt4O8TY8W0c47jzA7rEPQ4DLWFT9jjOxL-GeZOjaf4dkB91wbU4Iz1iJ70bCB8fzzP24Wp9e_mmuHn_-u3lq5uiVbWdi650tTC-aivVl12JgL2UTkjhPFiwEpyohe6sNQbbUgvZVpX3vpTe9kbXoM7Y80PulOKXXV6k2QZa9nQjxh01oECCMbLWmb44UJ8iUcK-mVLYunTXgGiWzpvceQOyWTrP-ukxeNdusftr_5ScwbMjcOTd0Cc3-kD_nIHSGjDZwcG1IZJfagt98O6_n_8CrQqbVQ</recordid><startdate>20130301</startdate><enddate>20130301</enddate><creator>Kuzmicki, Mariusz</creator><creator>Telejko, Beata</creator><creator>Wawrusiewicz-Kurylonek, Natalia</creator><creator>Lipinska, Danuta</creator><creator>Pliszka, Justyna</creator><creator>Wilk, Julisz</creator><creator>Zielinska, Anna</creator><creator>Skibicka, Justyna</creator><creator>Szamatowicz, Jacek</creator><creator>Kretowski, Adam</creator><creator>Gorska, M</creator><general>BioScientifica</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>20130301</creationdate><title>The expression of genes involved in NF-κB activation in peripheral blood mononuclear cells of patients with gestational diabetes</title><author>Kuzmicki, Mariusz ; Telejko, Beata ; Wawrusiewicz-Kurylonek, Natalia ; Lipinska, Danuta ; Pliszka, Justyna ; Wilk, Julisz ; Zielinska, Anna ; Skibicka, Justyna ; Szamatowicz, Jacek ; Kretowski, Adam ; Gorska, M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b398t-d5a907c6b63f5d5e1ef22a020ac181821a0904d8877eb5402b66ccc52c8f74913</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Adult</topic><topic>Biological and medical sciences</topic><topic>Blood Glucose - analysis</topic><topic>Chemokine CX3CL1 - genetics</topic><topic>Chemokine CX3CL1 - metabolism</topic><topic>Clinical Study</topic><topic>Diabetes, Gestational - blood</topic><topic>Diabetes, Gestational - diagnosis</topic><topic>Diabetes, Gestational - metabolism</topic><topic>Early Diagnosis</topic><topic>Endocrinopathies</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gene Expression Regulation</topic><topic>Humans</topic><topic>Insulin Resistance</topic><topic>Leukocytes, Mononuclear - metabolism</topic><topic>Medical sciences</topic><topic>NF-kappa B p50 Subunit - blood</topic><topic>NF-kappa B p50 Subunit - metabolism</topic><topic>PPAR gamma - genetics</topic><topic>PPAR gamma - metabolism</topic><topic>Pregnancy</topic><topic>Pregnancy Trimester, Second</topic><topic>Pregnancy Trimester, Third</topic><topic>Receptors, Tumor Necrosis Factor, Type I - genetics</topic><topic>Receptors, Tumor Necrosis Factor, Type I - metabolism</topic><topic>RNA, Messenger - metabolism</topic><topic>STAT Transcription Factors - genetics</topic><topic>STAT Transcription Factors - metabolism</topic><topic>Toll-Like Receptor 2 - genetics</topic><topic>Toll-Like Receptor 2 - metabolism</topic><topic>Toll-Like Receptor 4 - genetics</topic><topic>Toll-Like Receptor 4 - metabolism</topic><topic>Vertebrates: endocrinology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kuzmicki, Mariusz</creatorcontrib><creatorcontrib>Telejko, Beata</creatorcontrib><creatorcontrib>Wawrusiewicz-Kurylonek, Natalia</creatorcontrib><creatorcontrib>Lipinska, Danuta</creatorcontrib><creatorcontrib>Pliszka, Justyna</creatorcontrib><creatorcontrib>Wilk, Julisz</creatorcontrib><creatorcontrib>Zielinska, Anna</creatorcontrib><creatorcontrib>Skibicka, Justyna</creatorcontrib><creatorcontrib>Szamatowicz, Jacek</creatorcontrib><creatorcontrib>Kretowski, Adam</creatorcontrib><creatorcontrib>Gorska, 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>European journal of endocrinology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kuzmicki, Mariusz</au><au>Telejko, Beata</au><au>Wawrusiewicz-Kurylonek, Natalia</au><au>Lipinska, Danuta</au><au>Pliszka, Justyna</au><au>Wilk, Julisz</au><au>Zielinska, Anna</au><au>Skibicka, Justyna</au><au>Szamatowicz, Jacek</au><au>Kretowski, Adam</au><au>Gorska, M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The expression of genes involved in NF-κB activation in peripheral blood mononuclear cells of patients with gestational diabetes</atitle><jtitle>European journal of endocrinology</jtitle><addtitle>Eur J Endocrinol</addtitle><date>2013-03-01</date><risdate>2013</risdate><volume>168</volume><issue>3</issue><spage>419</spage><epage>427</epage><pages>419-427</pages><issn>0804-4643</issn><eissn>1479-683X</eissn><abstract>ObjectiveIn patients with obesity and type 2 diabetes, the changes in insulin resistance are associated with the changes in expression of genes involved in nuclear factor-κB (NF-κB) activation in peripheral blood mononuclear cells (PBMCs). As such studies have never been carried out in patients with gestational diabetes (GDM), in this study, we evaluated the expression of genes involved in NF-κB activation and related to glucose metabolism in PBMCs obtained from pregnant women with GDM and normal glucose tolerance (NGT).Design and methodsRT-PCR was performed in 60 pregnant women divided into three groups: GDM at the 1st visit, i.e. in the 24th–28th weeks of gestation (GDM1), NGT at the first visit and GDM in the 29th–32nd weeks (GDM2), and NGT at both visits. The tests were repeated 3 months postpartum.ResultsThe GDM1 group had significantly higher TLR2 (P=0.024), TLR4 (P=0.037), STAT1 (P=0.027), and CX3CL1 (P=0.017) mRNA expression, whereas the GDM2 group showed markedly lower TNFRSF1A (P=0.042), PPARG (P=0.018), STAT3 (P=0.013), and CX3CL1 (P=0.038) mRNA expression in comparison with the NGT group. The women with NGT at the 1st visit who later developed GDM had significantly higher fasting glucose (P=0.01), HOMA-IR (P=0.004), and TLR2 mRNA expression (P=0.04), as well as lower ISSI2 (P=0.01) and disposition indices, DI30 (P=0.03) and DI120 (P=0.01), than had the women who remained normoglycemic.ConclusionsOur results suggest that elevated TLR2 expression, as well as higher fasting glucose and lower compensation for increased insulin resistance, may represent early metabolic disturbances in the development of GDM.</abstract><cop>Bristol</cop><pub>BioScientifica</pub><pmid>23230212</pmid><doi>10.1530/EJE-12-0654</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record>
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source MEDLINE; Oxford University Press Journals All Titles (1996-Current)
subjects Adult
Biological and medical sciences
Blood Glucose - analysis
Chemokine CX3CL1 - genetics
Chemokine CX3CL1 - metabolism
Clinical Study
Diabetes, Gestational - blood
Diabetes, Gestational - diagnosis
Diabetes, Gestational - metabolism
Early Diagnosis
Endocrinopathies
Female
Fundamental and applied biological sciences. Psychology
Gene Expression Regulation
Humans
Insulin Resistance
Leukocytes, Mononuclear - metabolism
Medical sciences
NF-kappa B p50 Subunit - blood
NF-kappa B p50 Subunit - metabolism
PPAR gamma - genetics
PPAR gamma - metabolism
Pregnancy
Pregnancy Trimester, Second
Pregnancy Trimester, Third
Receptors, Tumor Necrosis Factor, Type I - genetics
Receptors, Tumor Necrosis Factor, Type I - metabolism
RNA, Messenger - metabolism
STAT Transcription Factors - genetics
STAT Transcription Factors - metabolism
Toll-Like Receptor 2 - genetics
Toll-Like Receptor 2 - metabolism
Toll-Like Receptor 4 - genetics
Toll-Like Receptor 4 - metabolism
Vertebrates: endocrinology
title The expression of genes involved in NF-κB activation in peripheral blood mononuclear cells of patients with gestational diabetes
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