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The Multifaceted Roles of Biomarkers in Metabolic Disorders: From Diagnosis...
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The Multifaceted Roles of Biomarkers in Metabolic Disorders: From Diagnosis and Monitoring to Prediction, Management, and Treatment

A special issue of Metabolites (ISSN 2218-1989). This special issue belongs to the section "Endocrinology and Clinical Metabolic Research".

Deadline for manuscript submissions: 15 August 2025 | Viewed by 3660

Special Issue Editors

Dr. Prince Dadson

E-Mail Website
Guest Editor
1. Turku PET Centre, University of Turku, Turku, Finland
2. Department of Clinical Medicine, University of Turku, Turku, Finland
Interests: obesity; metabolism; biomarkers; tissue metabolism; bariatric surgery studies; type 2 diabetes mellitus; eating disorders (anorexia nervosa); metabolic imaging
Dr. Miikka-Juhani Honka

E-Mail Website
Guest Editor
Turku PET Centre, University of Turku, Turku, Finland
Interests: metabolism; obesity; diabetes; MASLD; medical imaging; biomarkers

Special Issue Information

Dear Colleagues,

The increasing prevalence of metabolic disorders such as obesity, type 2 diabetes, and cardiovascular disease highlights the pressing need for innovative approaches to diagnosis, treatment, and prevention. The identification of functional biomarkers, including metabolites, microRNAs, and proteins, is crucial, as they can serve as early indicators of pathological dysfunction and damage, even before the onset of disease. Additionally, investigating the metabolic disturbances caused by drugs, nutrients, and environmental factors can elucidate the underlying biochemical pathways involved in these disorders and their complications. By developing novel analytical methods for biomarker analysis, we can gain valuable insights into tissue-specific metabolic disruptions, which could completely transform our understanding of the pathophysiology of metabolic disorders. Furthermore, studying biomarkers that predict treatment responses and integrating multi-biomarker data offer avenues for the implementation of personalized medicine strategies, ultimately leading to enhanced clinical outcomes. This comprehensive approach holds the potential to transform diagnostics, patient risk assessment, and therapeutic interventions for metabolic disorders. We welcome original research articles as well as in-depth reviews covering these topics.

Dr. Prince Dadson
Dr. Miikka-Juhani Honka
Guest Editors

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Keywords

  • metabolism
  • dysmetabolism
  • tissue-specific metabolism
  • cardiometabolic disorders
  • nutritional dis-orders
  • functional biomarkers
  • metabolomics profiling
  • multi-omics data integration
  • biochemical pathways
  • personalized medicine

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Published Papers (5 papers)

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Research

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13 pages, 1748 KiB  
Article
Lipidomic Signature of Pregnant and Postpartum Females by Longitudinal and Transversal Evaluation: Putative Biomarkers Determined by UHPLC-QTOF-ESI+-MS
by Alexandra Traila, Marius Craina, Carmen Socaciu, Andreea Iulia Socaciu, Diana Nitusca and Catalin Marian
Metabolites 2025, 15(1), 27; https://doi.org/10.3390/metabo15010027 - 8 Jan 2025
Viewed by 934
Abstract
Background: Pregnancy induces significant physiological and metabolic changes in the mother to support fetal growth and prepare for childbirth. These adaptations impact various systems, including immune tolerance, metabolism, and endocrine function. While metabolomics has been utilized to study pregnancy-related metabolic changes, comprehensive comparisons [...] Read more.
Background: Pregnancy induces significant physiological and metabolic changes in the mother to support fetal growth and prepare for childbirth. These adaptations impact various systems, including immune tolerance, metabolism, and endocrine function. While metabolomics has been utilized to study pregnancy-related metabolic changes, comprehensive comparisons between pregnant and non-pregnant states, particularly using ultra-high-performance liquid chromatography coupled with mass spectrometry (UHPLC-MS), remain limited. Methods: This study aimed to explore the dynamic, longitudinal metabolic shifts during pregnancy by profiling plasma samples from 65 pregnant women across three time points (6–14 weeks, 14–22 weeks, and >24 weeks) and 42 postpartum women. Lipidomics was prioritized, and a solvent mixture was employed to enhance lipid extraction, using UHPLC-QTOF-ESI+-MS. Results: A total of 290 metabolites were identified and analyzed. Our results revealed significant metabolic differences between pregnant and postpartum women, with lipid molecules such as estrogen derivatives, fatty acids, and ceramides showing strong potential as biomarkers. Further biomarker analysis highlighted distinct metabolic signatures between early and late pregnancy stages, particularly in lipid metabolism (with AUC values > 0.8). Conclusions: These findings contribute to a deeper understanding of pregnancy-related metabolic changes and may offer insights into maternal and neonatal health outcomes. Full article
(This article belongs to the Special Issue The Multifaceted Roles of Biomarkers in Metabolic Disorders: From Diagnosis and Monitoring to Prediction, Management, and Treatment)
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15 pages, 933 KiB  
Article
The Influence of Concurrent Autoimmune Thyroiditis on the Cardiometabolic Consequences of Cabergoline in Postmenopausal Women
by Robert Krysiak, Marcin Basiak, Witold Szkróbka and Bogusław Okopień
Metabolites 2025, 15(1), 9; https://doi.org/10.3390/metabo15010009 - 1 Jan 2025
Viewed by 1209
Abstract
Background: Untreated hyperprolactinemia and autoimmune thyroiditis (Hashimoto’s disease) seem to increase cardiometabolic risk. The cardiometabolic effects of cabergoline were less significant in young women with concurrent euthyroid Hashimoto’s illness. This study sought to investigate if the detrimental effects of this condition on cabergoline [...] Read more.
Background: Untreated hyperprolactinemia and autoimmune thyroiditis (Hashimoto’s disease) seem to increase cardiometabolic risk. The cardiometabolic effects of cabergoline were less significant in young women with concurrent euthyroid Hashimoto’s illness. This study sought to investigate if the detrimental effects of this condition on cabergoline efficacy are also evident in postmenopausal women. Methods: The study comprised 50 postmenopausal women exhibiting increased prolactin levels, with half qualifying for euthyroid Hashimoto’s illness. The subjects with thyroid autoimmunity were matched with those without thyroid disease according to age, body mass index, and prolactin levels. In addition to prolactin, we assessed thyroid-stimulating hormone (TSH), thyroid antibodies, and glucose homeostasis markers: fasting glucose, the homeostatic model assessment 1 of insulin resistance ratio (HOMA1-IR), and glycated hemoglobin (HbA1c). Furthermore, we assessed plasma lipids, plasma uric acid levels, high-sensitivity C-reactive protein (hsCRP), fibrinogen, homocysteine, and the urine albumin-to-creatinine ratio (UACR). The decadal cardiovascular risk was assessed with the Framingham Risk Score (FRS). Results: Before therapy, disparities existed among groups in HOMA1-IR, HDL cholesterol, antibody titers, uric acid, hsCRP, fibrinogen, homocysteine, UACR, and FRS. After six months of treatment, cabergoline successfully corrected prolactin levels (both total and monomeric) in women without thyroid disorders. This normalization correlated with decreases in HOMA1-IR, triglycerides, uric acid, hsCRP, fibrinogen, homocysteine, UACR, and FRS, as well as an elevation in HDL cholesterol. In women diagnosed with Hashimoto’s disease, cabergoline’s effects were limited to a reduction in prolactin levels, HOMA1-IR, and UACR, as well as an elevation in HDL cholesterol, with these alterations being less pronounced compared to women without thyroid illness. Conclusions: The cardiometabolic benefits of cabergoline were associated with the degree of prolactin concentration reduction. In women diagnosed with Hashimoto’s disease, connections were noted between baseline levels and treatment-induced alterations in hsCRP. These data indicate that concurrent euthyroid autoimmune thyroiditis mitigates the cardiometabolic consequences of cabergoline. Full article
(This article belongs to the Special Issue The Multifaceted Roles of Biomarkers in Metabolic Disorders: From Diagnosis and Monitoring to Prediction, Management, and Treatment)
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Review

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27 pages, 686 KiB  
Review
Fracture Risk in Chronic Kidney Disease: Addressing an Overlooked Complication
by Guido Gembillo, Concetto Sessa, Walter Morale, Luca Zanoli, Antonino Catalano, Salvatore Silipigni, Luca Soraci, Andrea Corsonello, Maria Princiotto, Carlo Lomonte and Domenico Santoro
Metabolites 2025, 15(7), 460; https://doi.org/10.3390/metabo15070460 - 7 Jul 2025
Viewed by 249
Abstract
Fracture risk is a serious yet underrecognized complication among patients with chronic kidney disease (CKD), especially in those with stages G3-G5D. The overlap between CKD-Mineral and Bone Disorder (CKD-MBD) and osteoporosis leads to complex bone changes that increase the likelihood of fragility fractures. [...] Read more.
Fracture risk is a serious yet underrecognized complication among patients with chronic kidney disease (CKD), especially in those with stages G3-G5D. The overlap between CKD-Mineral and Bone Disorder (CKD-MBD) and osteoporosis leads to complex bone changes that increase the likelihood of fragility fractures. Studies show that 18% to 32% of CKD patients also have osteoporosis, and these individuals are more than 2.5 times as likely to suffer from fractures compared to those without CKD. In the advanced stages of the disease, fracture risk is up to four times higher than in the general population, with the femur, forearm, and humerus being the most commonly affected sites. Hip fractures are of particular concern as they are linked to longer hospital stays and higher rates of morbidity and mortality. Furthermore, dialysis patients who experience hip fractures have a mortality rate 2.4 times higher than those in the general population with similar fractures. This increased risk underscores the need for proactive bone health maintenance in CKD patients to prevent fractures and related complications. This review explores the underlying pathophysiological mechanisms, diagnostic challenges, and treatment options related to bone fragility in CKD. Diagnostic tools, such as bone mineral density (BMD) assessments, the trabecular bone score (TBS), and biochemical markers, remain underused, especially in advanced CKD stages. Recent treatment strategies emphasize a multidisciplinary, stage-specific approach, incorporating calcium and vitamin D supplements, anti-resorptive agents like denosumab, and anabolic therapies such as teriparatide and romosozumab. Effective management needs to be tailored to the patient’s bone turnover status and stage of CKD. Despite progress in understanding bone fragility in CKD, significant gaps remain in both diagnosis and treatment. Personalized care, guided by updated KDIGO recommendations and based on an interdisciplinary approach, is essential to reduce fracture risk and improve outcomes in this vulnerable population. Further research is needed to validate risk assessment tools and refine therapeutic protocols. Full article
(This article belongs to the Special Issue The Multifaceted Roles of Biomarkers in Metabolic Disorders: From Diagnosis and Monitoring to Prediction, Management, and Treatment)
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21 pages, 1025 KiB  
Review
Amino Acid Metabolism in Liver Mitochondria: From Homeostasis to Disease
by Ranya Erdal, Kıvanç Birsoy and Gokhan Unlu
Metabolites 2025, 15(7), 446; https://doi.org/10.3390/metabo15070446 - 2 Jul 2025
Viewed by 341
Abstract
Hepatic mitochondria play critical roles in sustaining systemic nutrient balance, nitrogen detoxification, and cellular bioenergetics. These functions depend on tightly regulated mitochondrial processes, including amino acid catabolism, ammonia clearance via the urea cycle, and transport through specialized solute carriers. Genetic disruptions in these [...] Read more.
Hepatic mitochondria play critical roles in sustaining systemic nutrient balance, nitrogen detoxification, and cellular bioenergetics. These functions depend on tightly regulated mitochondrial processes, including amino acid catabolism, ammonia clearance via the urea cycle, and transport through specialized solute carriers. Genetic disruptions in these pathways underlie a range of inborn errors of metabolism, often resulting in systemic toxicity and neurological dysfunction. Here, we review the physiological functions of hepatic mitochondrial amino acid metabolism, with a focus on subcellular compartmentalization, disease mechanisms, and therapeutic strategies. We discuss how emerging genetic and metabolic interventions—including dietary modulation, cofactor replacement, and gene therapy—are reshaping treatment of liver-based metabolic disorders. Understanding these pathways offers mechanistic insights into metabolic homeostasis and reveals actionable vulnerabilities in metabolic disease and cancer. Full article
(This article belongs to the Special Issue The Multifaceted Roles of Biomarkers in Metabolic Disorders: From Diagnosis and Monitoring to Prediction, Management, and Treatment)
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Other

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10 pages, 625 KiB  
Case Report
Increased Lyso-Gb1 Levels in an Obese Splenectomized Gaucher Disease Type 1 Patient Treated with Eliglustat: Unacknowledged Poor Compliance or Underlying Factors
by Evelina Maines, Roberto Franceschi, Giacomo Luppi, Giacomo Marchi, Giovanni Piccoli, Nicola Vitturi, Massimo Soffiati, Annalisa Campomori and Silvana Anna Maria Urru
Metabolites 2025, 15(7), 427; https://doi.org/10.3390/metabo15070427 - 23 Jun 2025
Viewed by 290
Abstract
Eliglustat (Cerdelga®) is a potent and specific inhibitor of the enzyme glucosylceramide synthase and serves as a substrate reduction therapy for adult patients with Gaucher disease type 1 (GD1). It prevents the accumulation of several lipids, including glucosylsphingosine (also known as [...] Read more.
Eliglustat (Cerdelga®) is a potent and specific inhibitor of the enzyme glucosylceramide synthase and serves as a substrate reduction therapy for adult patients with Gaucher disease type 1 (GD1). It prevents the accumulation of several lipids, including glucosylsphingosine (also known as Lyso-Gb1). In addition to its role in diagnostics, Lyso-Gb1 has been proven to be a reliable biomarker for assessing disease severity and monitoring treatment efficacy. We present the case of an obese, splenectomized GD1 patient on long-term enzyme replacement therapy (ERT) who reported worsening fatigue and showed a progressive increase in Lyso-Gb1 levels after switching treatment from ERT to eliglustat. We provide a discussion of the potential clinical factors contributing to this outcome. As seen with ERT, Lyso-Gb1 levels during eliglustat treatment appear to respond earlier than other biochemical and clinical parameters. An increase in Lyso-Gb1 may signal early compromised clinical efficacy of the treatment. Data on biochemical and clinical outcomes in splenectomized or obese patients treated with eliglustat are limited, and the role of specific genotypes requires further clarification. The variability in responses to eliglustat highlights the complexity of GD and underscores the need for personalized approaches to treatment and monitoring. Full article
(This article belongs to the Special Issue The Multifaceted Roles of Biomarkers in Metabolic Disorders: From Diagnosis and Monitoring to Prediction, Management, and Treatment)
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