Ispir Emre, Saruhan Ercan, Topcu Deniz Ilhan, Varol Bugra, Akbaba Eren, Cakmak Tuba
Department of Medical Biochemistry, Bozyaka Research and Training Hospital, Izmir, Turkey.
Department of Medical Biochemistry, Faculty of Medicine, Mugla Sitki Kocman University, Mugla, Turkey.
Placenta. 2025 Jan;159:119-125. doi: 10.1016/j.placenta.2024.12.007. Epub 2024 Dec 12.
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.
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.
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).
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.
妊娠期糖尿病（GDM）被定义为孕期出现的葡萄糖不耐受。我们旨在研究β细胞生成素和载脂蛋白C2（ApoC2）在妊娠期糖尿病中的潜在作用，重点关注它们在脂蛋白脂肪酶（LPL）调节中的作用以及它们与胎盘催乳素（hPL）的关系，以阐明hPL对脂质代谢的可能影响及其对妊娠期糖尿病发展的潜在作用。
本研究纳入了30名糖耐量正常的孕妇和29名妊娠期糖尿病患者（通过24至28周的75克口服葡萄糖耐量试验诊断）。采用酶联免疫吸附测定法（ELISA）检测血清β细胞生成素、hPL和ApoC2，并计算胰岛素抵抗指数（HOMA-IR）。
在妊娠期糖尿病组中，hPL水平与β细胞生成素和ApoC2相关（r = 0.552，p < 0.05；r = 0.588，p < 0.05），而β细胞生成素与ApoC2相关（r = 0.584，p < 0.05）。在对照组中，观察到hPL与β细胞生成素之间以及hPL与ApoC2值之间存在线性关系（r分别为0.454，p < 0.05；r = 0.779，p < 0.01）。胰岛素抵抗指数（HOMA-IR）临界值>2.5的妊娠期糖尿病组（n = 20）的ApoC2水平显著高于对照组（n = 10）（p < 0.05）。β细胞生成素与ApoC2之间也存在正相关关系（r = 0.591）（p < 0.05）。
妊娠期糖尿病患者除胰岛素抵抗外，可能存在脂蛋白脂肪酶（LPL）酶调节受损，hPL可能促成了这种破坏。脂蛋白脂肪酶活性受损及其继发于遗传疾病的失调可能在妊娠期糖尿病的发病机制中起作用。进一步研究不同类型糖尿病患者中β细胞生成素、ApoC2和其他LPL调节剂之间的相关性，可能有助于更全面地理解这种相互作用。
