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Background <p>As global obesity rates rise, women are disproportionately affected, placing them at elevated risk for both metabolic dysfunction and cardiovascular complications. This study investigated the expression of <i>Krüppel-like</i> transcription factors <i>KLF4</i> and <i>KLF5</i> in visceral adipose tissue (VAT) from obese women to explore their potential roles in the pathogenesis of metabolic dysfunction.</p> Methods <p>In this case–control study, 46 women undergoing laparoscopic surgery were categorized into obese (<i>n</i> = 24) and non-obese control (<i>n</i> = 22) groups. VAT samples were analyzed for <i>KLF4</i> and <i>KLF5</i> mRNA expression using quantitative RT-PCR, normalized to <i>GAPDH</i>. Serum biomarkers related to glycemic status, lipid metabolism, adiposity indices, and cardiovascular risk were measured with automated clinical analyzers. Gene expression was correlated with metabolic parameters using Pearson and Spearman tests, with false discovery rate (FDR) correction for multiple comparisons.</p> Results <p><i>KLF4</i> and <i>KLF5</i> expression levels did not differ significantly between groups. However, in the obese group, <i>KLF4</i> expression showed positive correlations with HOMA-IR, HbA1c, fasting insulin, and glucose—indicating links to insulin resistance and glycemic regulation. In contrast, <i>KLF5</i> expression was associated with lipid-related and cardiovascular parameters, including LDL-C, total cholesterol, CK-MB, and waist-to-hip ratio. In non-obese women, <i>KLF4</i> and <i>KLF5</i> exhibited coordinated expression, though their associations with metabolic traits were less pronounced. These findings indicate a BMI-dependent modulation of the <i>KLF4/KLF5</i> regulatory axis, with obesity amplifying its links to dysglycemia and dyslipidemia.</p> Conclusion <p>The <i>KLF4/KLF5</i> transcriptional axis exhibits obesity-related regulatory shifts that may contribute to cardiometabolic dysfunction. These patterns highlight the potential utility of <i>KLF4</i> and <i>KLF5</i> as biomarkers for risk stratification, informing the development of tissue-specific therapeutic strategies aimed at improving metabolic outcomes in obese women, while ensuring that translational approaches remain safe, equitable, and targeted.</p>

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Gene expression profiling of KLF4 and KLF5 in visceral adipose tissue of obese women: insights into adipogenic and metabolic regulation

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年10月16日

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  • Dalya Jamal Muhi,
  • Maher Mohammed Murad,
  • Ghodratollah Panahi,
  • Hossein Zabihi-Mahmoudabadi,
  • Solaleh Emamgholipour,
  • Azin Nowrouzi

摘要

Background

As global obesity rates rise, women are disproportionately affected, placing them at elevated risk for both metabolic dysfunction and cardiovascular complications. This study investigated the expression of Krüppel-like transcription factors KLF4 and KLF5 in visceral adipose tissue (VAT) from obese women to explore their potential roles in the pathogenesis of metabolic dysfunction.

Methods

In this case–control study, 46 women undergoing laparoscopic surgery were categorized into obese (n = 24) and non-obese control (n = 22) groups. VAT samples were analyzed for KLF4 and KLF5 mRNA expression using quantitative RT-PCR, normalized to GAPDH. Serum biomarkers related to glycemic status, lipid metabolism, adiposity indices, and cardiovascular risk were measured with automated clinical analyzers. Gene expression was correlated with metabolic parameters using Pearson and Spearman tests, with false discovery rate (FDR) correction for multiple comparisons.

Results

KLF4 and KLF5 expression levels did not differ significantly between groups. However, in the obese group, KLF4 expression showed positive correlations with HOMA-IR, HbA1c, fasting insulin, and glucose—indicating links to insulin resistance and glycemic regulation. In contrast, KLF5 expression was associated with lipid-related and cardiovascular parameters, including LDL-C, total cholesterol, CK-MB, and waist-to-hip ratio. In non-obese women, KLF4 and KLF5 exhibited coordinated expression, though their associations with metabolic traits were less pronounced. These findings indicate a BMI-dependent modulation of the KLF4/KLF5 regulatory axis, with obesity amplifying its links to dysglycemia and dyslipidemia.

Conclusion

The KLF4/KLF5 transcriptional axis exhibits obesity-related regulatory shifts that may contribute to cardiometabolic dysfunction. These patterns highlight the potential utility of KLF4 and KLF5 as biomarkers for risk stratification, informing the development of tissue-specific therapeutic strategies aimed at improving metabolic outcomes in obese women, while ensuring that translational approaches remain safe, equitable, and targeted.