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Introduction <p>Diabetic foot ulcer (DFU) is a severe complication of diabetes mellitus (DM) characterized by chronic inflammation, impaired wound repair, and systemic metabolic imbalance. This study aimed to identify plasma metabolite signatures associated with DFU and investigate altered metabolic pathways that may serve as potential biomarker.</p> Objective <p>The study aims to identify metabolic alterations and potential biomarkers associated with diabetic foot ulcers, with a focus on the role of vitamin D.</p> Methods <p>We performed an LC/MS/MS-based untargeted metabolomic profiling on plasma sample from DFU patients (<i>n</i> = 22), DM patients without foot ulcers (<i>n</i> = 22), and healthy controls (<i>n</i> = 10). The mean age group was 54years, with comparable gender (male = 9; female = 13) distribution in DFU and DM groups.</p> Results <p>PLS-DA showed clear metabolic separation between DFU and DM groups. DFU group showed elevated levels of aspartic acid, glutamic acid, taurine, and D-fructose, indicating altered hyperglycemia induced metabolic stress. In contrast, calcitriol and glutathione were significantly reduced (<i>P</i> &lt; 0.01), suggesting compromised antioxidant capacity and immune metabolic regulation. Downregulation of sphingosine-1-phosphate (SIP), <span>l</span>-palmitoylcarnitine, and docosahexaenoic acid (DHA) suggest disruptions in mitochondrial dynamics, and wound healing. Elevated taurine, potentially regulated by the vitamin D receptor (VDR), links vitamin D to tissue homeostasis.</p> Conclusions <p>This study reveals coordinated disturbances in lipid metabolism, antioxidant defense, and vitamin D signaling in DFU. The identified metabolite signatures highlight pathway-level metabolic alterations associated with impaired wound healing. Our findings suggest that the biological impact of vitamin D in DFU may depend not only on supplementation, but also on its downstream conversion to calcitriol.</p>

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Metabolomic profiling and vitamin D pathway investigation in diabetic foot ulcer patients

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月13日

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  • Remya Reveendran,
  • Sreelathakumari Krishnan Thankam,
  • Adbul Jaleel,
  • Arun Surendran,
  • Sara Jones,
  • Suchithra Tharamel Vasu

摘要

Introduction

Diabetic foot ulcer (DFU) is a severe complication of diabetes mellitus (DM) characterized by chronic inflammation, impaired wound repair, and systemic metabolic imbalance. This study aimed to identify plasma metabolite signatures associated with DFU and investigate altered metabolic pathways that may serve as potential biomarker.

Objective

The study aims to identify metabolic alterations and potential biomarkers associated with diabetic foot ulcers, with a focus on the role of vitamin D.

Methods

We performed an LC/MS/MS-based untargeted metabolomic profiling on plasma sample from DFU patients (n = 22), DM patients without foot ulcers (n = 22), and healthy controls (n = 10). The mean age group was 54years, with comparable gender (male = 9; female = 13) distribution in DFU and DM groups.

Results

PLS-DA showed clear metabolic separation between DFU and DM groups. DFU group showed elevated levels of aspartic acid, glutamic acid, taurine, and D-fructose, indicating altered hyperglycemia induced metabolic stress. In contrast, calcitriol and glutathione were significantly reduced (P < 0.01), suggesting compromised antioxidant capacity and immune metabolic regulation. Downregulation of sphingosine-1-phosphate (SIP), l-palmitoylcarnitine, and docosahexaenoic acid (DHA) suggest disruptions in mitochondrial dynamics, and wound healing. Elevated taurine, potentially regulated by the vitamin D receptor (VDR), links vitamin D to tissue homeostasis.

Conclusions

This study reveals coordinated disturbances in lipid metabolism, antioxidant defense, and vitamin D signaling in DFU. The identified metabolite signatures highlight pathway-level metabolic alterations associated with impaired wound healing. Our findings suggest that the biological impact of vitamin D in DFU may depend not only on supplementation, but also on its downstream conversion to calcitriol.