Emre Ispir, Ercan Saruhan, Deniz Ilhan Topcu, Bugra Varol, Eren Akbaba, Tuba Cakmak
{"title":"妊娠糖尿病患者血清中ANGPTL8、载脂蛋白C2和人胎盘泌乳素(hPL)水平之间的关系:LPL调节剂与hPL的相互作用,可能是导致胰岛素抵抗的一个因素。","authors":"Emre Ispir, Ercan Saruhan, Deniz Ilhan Topcu, Bugra Varol, Eren Akbaba, Tuba Cakmak","doi":"10.1016/j.placenta.2024.12.007","DOIUrl":null,"url":null,"abstract":"<p><strong>Introduction: </strong>Gestational diabetes mellitus (GDM) is defined as glucose intolerance during pregnancy. We aimed to investigate the potential effects of betatrophin and ApoC2 in GDM, focusing on their roles in LPL (lipoprotein lipase) regulation and their relationship with hPL to elucidate the possible impact of hPL on lipid metabolism and its potential contribution to the development of GDM.</p><p><strong>Methods: </strong>Thirty pregnant women with normal glucose tolerance and 29 with gestational diabetes mellitus (diagnosed by 75g OGTT between 24 and 28 weeks) were included in the study. Serum betatrophin, hPL, and ApoC2 were measured by Elisa and HOMA-IR was calculated.</p><p><strong>Results: </strong>In the GDM group, hPL levels correlated with betatrophin and ApoC2 (r = 0.552, p < 0.05; r = 0.588, p < 0.05 respectively) while betatrophin correlated with the ApoC2 (r = 0.584, p < 0.05). A linear relationship between hPL and betatropin and also between hPL and ApoC2 values in the control group (r = 0.454, p < 0.05; r = 0.779, p < 0.01 respectively) were observed. ApoC2 levels in the GDM group (n = 20) with HOMA-IR cut-off >2.5 were significantly higher than the control group (n = 10) (p < 0.05). There was also a positive relationship between betatrophin and ApoC2 (r = 0.591) (p < 0.05).</p><p><strong>Discussion: </strong>GDM patients may have impaired LPL enzyme regulation in addition to insulin resistance, with hPL potentially contributing to this disruption. Impaired lipoprotein lipase activity and its dysregulation secondary to genetic disorders may play a role in the etiopathogenesis of GDM. Further investigation into the correlation between betatrophin, ApoC2, and other LPL modulators in patients with various forms of diabetes could be beneficial for understanding this interaction more comprehensively.</p>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":"159 ","pages":"119-125"},"PeriodicalIF":3.0000,"publicationDate":"2024-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Relationship between serum levels of ANGPTL8, Apo C2, and human placental lactogen (hPL) in patients with gestational diabetes mellitus: Interaction of LPL regulators with hPL, a possible contributing factor to insulin resistance.\",\"authors\":\"Emre Ispir, Ercan Saruhan, Deniz Ilhan Topcu, Bugra Varol, Eren Akbaba, Tuba Cakmak\",\"doi\":\"10.1016/j.placenta.2024.12.007\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Introduction: </strong>Gestational diabetes mellitus (GDM) is defined as glucose intolerance during pregnancy. We aimed to investigate the potential effects of betatrophin and ApoC2 in GDM, focusing on their roles in LPL (lipoprotein lipase) regulation and their relationship with hPL to elucidate the possible impact of hPL on lipid metabolism and its potential contribution to the development of GDM.</p><p><strong>Methods: </strong>Thirty pregnant women with normal glucose tolerance and 29 with gestational diabetes mellitus (diagnosed by 75g OGTT between 24 and 28 weeks) were included in the study. Serum betatrophin, hPL, and ApoC2 were measured by Elisa and HOMA-IR was calculated.</p><p><strong>Results: </strong>In the GDM group, hPL levels correlated with betatrophin and ApoC2 (r = 0.552, p < 0.05; r = 0.588, p < 0.05 respectively) while betatrophin correlated with the ApoC2 (r = 0.584, p < 0.05). A linear relationship between hPL and betatropin and also between hPL and ApoC2 values in the control group (r = 0.454, p < 0.05; r = 0.779, p < 0.01 respectively) were observed. ApoC2 levels in the GDM group (n = 20) with HOMA-IR cut-off >2.5 were significantly higher than the control group (n = 10) (p < 0.05). There was also a positive relationship between betatrophin and ApoC2 (r = 0.591) (p < 0.05).</p><p><strong>Discussion: </strong>GDM patients may have impaired LPL enzyme regulation in addition to insulin resistance, with hPL potentially contributing to this disruption. Impaired lipoprotein lipase activity and its dysregulation secondary to genetic disorders may play a role in the etiopathogenesis of GDM. Further investigation into the correlation between betatrophin, ApoC2, and other LPL modulators in patients with various forms of diabetes could be beneficial for understanding this interaction more comprehensively.</p>\",\"PeriodicalId\":20203,\"journal\":{\"name\":\"Placenta\",\"volume\":\"159 \",\"pages\":\"119-125\"},\"PeriodicalIF\":3.0000,\"publicationDate\":\"2024-12-12\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Placenta\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1016/j.placenta.2024.12.007\",\"RegionNum\":2,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"DEVELOPMENTAL BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Placenta","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1016/j.placenta.2024.12.007","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"DEVELOPMENTAL BIOLOGY","Score":null,"Total":0}
Relationship between serum levels of ANGPTL8, Apo C2, and human placental lactogen (hPL) in patients with gestational diabetes mellitus: Interaction of LPL regulators with hPL, a possible contributing factor to insulin resistance.
Introduction: Gestational diabetes mellitus (GDM) is defined as glucose intolerance during pregnancy. We aimed to investigate the potential effects of betatrophin and ApoC2 in GDM, focusing on their roles in LPL (lipoprotein lipase) regulation and their relationship with hPL to elucidate the possible impact of hPL on lipid metabolism and its potential contribution to the development of GDM.
Methods: Thirty pregnant women with normal glucose tolerance and 29 with gestational diabetes mellitus (diagnosed by 75g OGTT between 24 and 28 weeks) were included in the study. Serum betatrophin, hPL, and ApoC2 were measured by Elisa and HOMA-IR was calculated.
Results: In the GDM group, hPL levels correlated with betatrophin and ApoC2 (r = 0.552, p < 0.05; r = 0.588, p < 0.05 respectively) while betatrophin correlated with the ApoC2 (r = 0.584, p < 0.05). A linear relationship between hPL and betatropin and also between hPL and ApoC2 values in the control group (r = 0.454, p < 0.05; r = 0.779, p < 0.01 respectively) were observed. ApoC2 levels in the GDM group (n = 20) with HOMA-IR cut-off >2.5 were significantly higher than the control group (n = 10) (p < 0.05). There was also a positive relationship between betatrophin and ApoC2 (r = 0.591) (p < 0.05).
Discussion: GDM patients may have impaired LPL enzyme regulation in addition to insulin resistance, with hPL potentially contributing to this disruption. Impaired lipoprotein lipase activity and its dysregulation secondary to genetic disorders may play a role in the etiopathogenesis of GDM. Further investigation into the correlation between betatrophin, ApoC2, and other LPL modulators in patients with various forms of diabetes could be beneficial for understanding this interaction more comprehensively.
期刊介绍:
Placenta publishes high-quality original articles and invited topical reviews on all aspects of human and animal placentation, and the interactions between the mother, the placenta and fetal development. Topics covered include evolution, development, genetics and epigenetics, stem cells, metabolism, transport, immunology, pathology, pharmacology, cell and molecular biology, and developmental programming. The Editors welcome studies on implantation and the endometrium, comparative placentation, the uterine and umbilical circulations, the relationship between fetal and placental development, clinical aspects of altered placental development or function, the placental membranes, the influence of paternal factors on placental development or function, and the assessment of biomarkers of placental disorders.