Scholarlink

Background and aims <p>Gestational diabetes mellitus (GDM) is defined as glucose intolerance first identified during pregnancy that does not meet the criteria for overt diabetes. Its pathophysiology shares key features with type 2 diabetes mellitus (T2D), including insulin resistance and inflammation. Emerging evidence suggests that long non-coding RNAs (lncRNAs) are implicated in T2D. This study investigates the gene expression of lncRNAs in GDM and explores their association with insulin resistance and proinflammatory cytokines.</p> Materials and methods <p>This cross-sectional study included 25 GDM and 36 non-GDM (NGDM) participants from a tertiary care antenatal clinic. GDM was diagnosed using a 75&#xa0;g oral glucose tolerance test (OGTT) based on the International Association of Diabetes and Pregnancy Study Groups criteria. MALAT1, MEG3, and XIST were selected for analysis due to their reported involvement in T2D. Their gene expression levels were quantified using real-time PCR, while serum concentrations of proinflammatory cytokines (TNF-α, IL-6, IL-1β) and glycemic markers (C-peptide, fasting insulin) were measured using ELISA.</p> Results <p>MALAT1, MEG3, and XIST were significantly downregulated in the GDM group compared to the NGDM group (<i>p</i> &lt; 0.01). In the GDM group, all three lncRNAs showed a significant negative correlation with Homeostasis Model Assessment for Insulin Resistance (HOMA-IR) (MALAT1: <i>r</i> = -0.44, <i>p</i> = 0.03; MEG3: <i>r</i> = -0.46, <i>p</i> = 0.04; XIST: <i>r</i> = -0.45, <i>p</i> = 0.04). Additionally, MALAT1 gene expression negatively correlated with IL-6 (<i>r</i> = -0.49, <i>p</i> = 0.03) and TNF-α (<i>r</i> = -0.48, <i>p</i> = 0.04). MEG3 and XIST gene expression negatively correlated with IL-1β (<i>r</i> = -0.51 and − 0.50, <i>p</i> = 0.03 for both) and TNF-α (<i>r</i> = -0.47 and − 0.52, <i>p</i> = 0.04 and 0.03, respectively).</p> Conclusion <p>MALAT1, MEG3, and XIST are downregulated in GDM, and their gene expression levels are negatively correlated with insulin resistance and select proinflammatory cytokines. These findings suggest a potential role for lncRNA downregulation in GDM pathogenesis, warranting further investigation.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Expression of long non-coding RNAs MALAT1, MEG3, and XIST in gestational diabetes mellitus: a cross-sectional study

  • 期刊论文

  • 发表日期：

    2025年9月10日

查看全文
  • Bishal Kumar Dey,
  • Sudipta Banerjee,
  • Pieu Adhikary,
  • Subhankar Chowdhury,
  • Sanchita Roy,
  • Subesha Basu Roy,
  • Rana Bhattacharjee

摘要

Background and aims

Gestational diabetes mellitus (GDM) is defined as glucose intolerance first identified during pregnancy that does not meet the criteria for overt diabetes. Its pathophysiology shares key features with type 2 diabetes mellitus (T2D), including insulin resistance and inflammation. Emerging evidence suggests that long non-coding RNAs (lncRNAs) are implicated in T2D. This study investigates the gene expression of lncRNAs in GDM and explores their association with insulin resistance and proinflammatory cytokines.

Materials and methods

This cross-sectional study included 25 GDM and 36 non-GDM (NGDM) participants from a tertiary care antenatal clinic. GDM was diagnosed using a 75 g oral glucose tolerance test (OGTT) based on the International Association of Diabetes and Pregnancy Study Groups criteria. MALAT1, MEG3, and XIST were selected for analysis due to their reported involvement in T2D. Their gene expression levels were quantified using real-time PCR, while serum concentrations of proinflammatory cytokines (TNF-α, IL-6, IL-1β) and glycemic markers (C-peptide, fasting insulin) were measured using ELISA.

Results

MALAT1, MEG3, and XIST were significantly downregulated in the GDM group compared to the NGDM group (p < 0.01). In the GDM group, all three lncRNAs showed a significant negative correlation with Homeostasis Model Assessment for Insulin Resistance (HOMA-IR) (MALAT1: r = -0.44, p = 0.03; MEG3: r = -0.46, p = 0.04; XIST: r = -0.45, p = 0.04). Additionally, MALAT1 gene expression negatively correlated with IL-6 (r = -0.49, p = 0.03) and TNF-α (r = -0.48, p = 0.04). MEG3 and XIST gene expression negatively correlated with IL-1β (r = -0.51 and − 0.50, p = 0.03 for both) and TNF-α (r = -0.47 and − 0.52, p = 0.04 and 0.03, respectively).

Conclusion

MALAT1, MEG3, and XIST are downregulated in GDM, and their gene expression levels are negatively correlated with insulin resistance and select proinflammatory cytokines. These findings suggest a potential role for lncRNA downregulation in GDM pathogenesis, warranting further investigation.