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Metabolites
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Lipid Metabolism Dysregulation in Metabolic Disorders: Unraveling the Molecular Complexity
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Lipid Metabolism Dysregulation in Metabolic Disorders: Unraveling the Molecular Complexity

A special issue of Metabolites (ISSN 2218-1989). This special issue belongs to the section "Lipid Metabolism".

Deadline for manuscript submissions: 30 April 2026 | Viewed by 5606

Special Issue Editor

Dr. Joshua De Leon

E-Mail Website
Guest Editor
1. Department of Medicine, NYU Long Island School of Medicine, Mineola, New York, NY 11501, USA
2. Division of Cardiology, Department of Medicine, NYU Long Island School of Medicine, Mineola, NY 11501, USA
Interests: inflammation; lipids; cardio-neurologic axis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Lipid metabolism and homeostasis are critical for the proper functioning of multiple organ systems, particularly for the cardiovascular and nervous systems. Disorders of lipid metabolism may begin early in life or manifest in older people, and the consequences can be devastating. Dysregulated lipid production, processing, and storage can result from specific genetic mutations or complex multifactorial processes and may also be environmentally influenced. This Special Issue accepts submissions on a wide range of topics related to lipid abnormalities spanning organ systems, life stage, and etiology. Articles focused on dyslipidemia, obesity, diabetes, atherosclerosis, and the effects of chronic inflammation on the heart and brain are welcome, as are those covering dysfunction of hepatic lipid metabolism. Papers that focus on mechanistic aspects, molecular pathways, and innovative therapies are of particular interest. Both review articles and original research will be considered.

Dr. Joshua De Leon
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Metabolites is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • lipid metabolism
  • dyslipidemia
  • atherosclerosis

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Published Papers (4 papers)

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Research

20 pages, 8426 KB  
Article
Metabolomic Profile of Weight Gain of People Living with HIV Treated with Integrase Strand Transfer Inhibitor Regimens Reveals Dysregulated Lipid Metabolism and Mitochondrial Dysfunction
by Ana Miriam Ascencio-Anastacio, Violeta Larios-Serrato, José Antonio Mata-Marín, Mara Rodríguez Evaristo, Mireya Núñez-Armendáriz, Ana Luz Cano-Díaz, Alberto Chaparro-Sánchez, Gloria Elizabeth Salinas-Velázquez, Angélica Maldonado-Rodríguez, Javier Torres, María Martha García-Flores, Zuriel Eduardo Martínez-Valencia, Beatriz Irene Arroyo-Sánchez, Viridiana Olin-Sandoval, Fernando Minauro, Jesus Enrique Gaytán-Martínez and Ericka Nelly Pompa-Mera
Metabolites 2025, 15(11), 695; https://doi.org/10.3390/metabo15110695 - 25 Oct 2025
Viewed by 946
Abstract
Background/Objectives: Excessive weight gain is a growing concern among people living with HIV (PWH) receiving integrase strand transfer inhibitor (INSTI)-based regimens as first-line antiretroviral therapy (ART), as it may contribute to multimorbidity. The mechanisms driving weight gain in INSTI users are not [...] Read more.
Background/Objectives: Excessive weight gain is a growing concern among people living with HIV (PWH) receiving integrase strand transfer inhibitor (INSTI)-based regimens as first-line antiretroviral therapy (ART), as it may contribute to multimorbidity. The mechanisms driving weight gain in INSTI users are not fully understood but are thought to be multifactorial. This study examines the plasma metabolome associated with weight gain in PWH on INSTI-based regimens. Methods: We conducted a nested case–control study within the randomized clinical trial MICTLAN (NCT06629480). Sixty-six participants were randomized to receive INSTI-based regimens, either bictegravir/tenofovir alafenamide/emtricitabine (BIC/TAF/FTC) or dolutegravir/abacavir/lamivudine (DTG/ABC/3TC), and followed for 18 months. Weight gain >10% relative to baseline was considered a primary endpoint and used as a criterium to categorize cases (n = 28) and controls (n = 38). Anthropometric and clinical measurements, plasma insulin, and metabolomic profiles were assessed at baseline and 18 months post-ART. Plasma untargeted metabolomics was performed using liquid chromatography–mass spectrometry (LC-MS/MS) to identify metabolomic changes linked to weight gain. Bioinformatic tools, including Partial Least Squares Discriminant Analysis (PLS-DA), volcano plots, and KEGG pathway enrichment analysis, were used to analyze plasma metabolomes and identify significant differential metabolites. Results: Weight gain at 18 months in PWH on INSTI-based ART was associated with insulin resistance, as measured by HOMA-IR (OR 3.23; 95% CI 1.14–9.10; p = 0.023), and visceral adipose tissue thickness > 4 cm (OR 4.50; 95% CI 1.60–13.03; 9.10; p = 0.004), and hypertriglyceridemia (OR 3.9; 95% CI 1.38–10.94; p = 0.008). Baseline HIV RNA viral load >50,000 copies/mL (OR 8.05; 95% CI 2.65–24.43; p = 0.0002) was identified as a baseline predictor of weight gain (aOR 6.58 (1.83–23.58); p = 0.004). In addition, accumulation of circulating medium-chain acylcarnitines, indicative of mitochondrial dysfunction, and insulin resistance were linked to weight gain in PWH on INSTI-based regimens after 18 months of therapy. Conclusions: This metabolomic study identified metabolites reflecting mitochondrial dysfunction, dysregulated lipid metabolism, and altered amino acid metabolism as key mechanisms underlying insulin resistance and weight gain in PWH on INSTI-based ART. Full article
(This article belongs to the Special Issue Lipid Metabolism Dysregulation in Metabolic Disorders: Unraveling the Molecular Complexity)
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16 pages, 3103 KB  
Article
Plasma Lipidomic Alterations in Fontan Circulation Reflect Cardiovascular Functional Reserve
by Arun Surendran, Amir Ravandi and Ashish H. Shah
Metabolites 2025, 15(9), 592; https://doi.org/10.3390/metabo15090592 - 7 Sep 2025
Viewed by 692
Abstract
Background: Fontan circulation is associated with impaired cardiac output, reduced exercise capacity, and systemic metabolic stress. However, the underlying lipidomic alterations remain poorly defined. Methods: Using targeted mass spectrometry, we analyzed 291 lipid species in fasting plasma samples from 20 adults with Fontan [...] Read more.
Background: Fontan circulation is associated with impaired cardiac output, reduced exercise capacity, and systemic metabolic stress. However, the underlying lipidomic alterations remain poorly defined. Methods: Using targeted mass spectrometry, we analyzed 291 lipid species in fasting plasma samples from 20 adults with Fontan circulation and 20 age- and sex-matched healthy controls. Results: Forty-eight lipids were significantly altered between groups (p < 0.05), including reductions in total lysophosphatidylcholines (LPC) and total ether-linked LPC [LPC(O)] and elevations in total phosphatidylserines (PS). Notably, LPC(O-22:1) and LPC(O-20:0) were decreased, while PS 40:5 was elevated, with several of these species demonstrating strong correlations (|r| > 0.5, p < 0.001) with the stroke index, cardiac index, and VO2max. These three lipid species also showed excellent capability in discriminating Fontan patients from healthy controls (AUC > 0.78). Correlation network and pathway enrichment analyses revealed tightly coordinated lipid clusters containing LPC/LPC(O), PE, and PS species as central features of dysregulated Fontan metabolism. Conclusions: These exploratory findings highlight coordinated lipid alterations associated with impaired cardiovascular reserve in Fontan patients. While based on unadjusted p-values and therefore being hypothesis-generating, they provide novel insight into the metabolic landscape of Fontan physiology and warrant validation in larger, independent cohorts. Full article
(This article belongs to the Special Issue Lipid Metabolism Dysregulation in Metabolic Disorders: Unraveling the Molecular Complexity)
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17 pages, 1684 KB  
Article
Dietary Nicotinamide Mononucleotide, a Key NAD+ Intermediate, Alleviates Body Fat Mass and Hypertriglyceridemia by Enhancing Energy Expenditure with Promotion of Fat Oxidation and Hepatic Lipolysis and Suppressing Hepatic Lipogenesis in db/db Mice
by Bungo Shirouchi, Sarasa Mitsuta, Mina Higuchi, Mai Okumura and Kazunari Tanaka
Metabolites 2025, 15(5), 333; https://doi.org/10.3390/metabo15050333 - 18 May 2025
Viewed by 1906
Abstract
Background/Objectives: Supplementation with nicotinamide mononucleotide (NMN), a key nicotinamide adenine dinucleotide (NAD+) intermediate, exerts anti-aging, anti-obesity, and anti-diabetic effects in animal experiments. However, previous studies have evaluated NMN supplementation using oral administration in drinking water or by intraperitoneal administration. No [...] Read more.
Background/Objectives: Supplementation with nicotinamide mononucleotide (NMN), a key nicotinamide adenine dinucleotide (NAD+) intermediate, exerts anti-aging, anti-obesity, and anti-diabetic effects in animal experiments. However, previous studies have evaluated NMN supplementation using oral administration in drinking water or by intraperitoneal administration. No studies have reported whether NMN exerts beneficial effects when incorporated into the diet. The diet is a multicomponent mixture of many nutrients that may interact with each other, thus weakening the effects of NMN. In the present study, we evaluated whether dietary NMN intake protects obese diabetic db/db mice from obesity-related metabolic disorders, such as dyslipidemia, hepatic steatosis, hyperglycemia, and hyperinsulinemia. Methods: Five-week-old male db/db mice were randomly assigned to two groups and fed for four weeks either a control diet containing 7% corn oil and 0.1% cholesterol (CON group, n = 6) or a diet supplemented with 0.5% NMN (NMN group, n = 5). Results: After 4 weeks of feeding, dietary NMN intake alleviated obesity, hypertriglyceridemia, and hepatic triglyceride accumulation in db/db mice. Respiratory gas analysis indicated that dietary NMN intake significantly enhanced energy expenditure by suppressing carbohydrate oxidation and increasing fat oxidation after 3 weeks of feeding. Additionally, the suppression of the increase in plasma triglyceride (TG) levels by dietary NMN intake was attributable to a reduction in hepatic TG levels through the suppression of fatty acid synthesis and the enhancement of fatty acid β-oxidation in the liver. Furthermore, the improvement in hepatic fatty acid metabolism induced by dietary NMN intake was partially responsible for the significant increase in plasma adiponectin and soluble T-cadherin levels. Conclusions: This is the first report to show that dietary NMN intake but not oral administration in drinking water or intraperitoneal administration alleviates body fat mass and hypertriglyceridemia by enhancing energy expenditure, with preferential promotion of fat oxidation, the enhancement of hepatic lipolysis, and the suppression of hepatic lipogenesis in db/db mice. Full article
(This article belongs to the Special Issue Lipid Metabolism Dysregulation in Metabolic Disorders: Unraveling the Molecular Complexity)
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13 pages, 253 KB  
Article
The Effects of SGLT2 Inhibitors on Lipid Profile and Kidney Function in Patients with Chronic Kidney Disease Regardless of Diabetes and Hypertension Status
by Selena Gajić, Stefan Janković, Milorad Stojadinović, Kristina Filić, Ana Bontić, Jelena Pavlović, Ivana Mrđa, Kristina Petrović, Lara Hadži-Tanović, Jelena Žunić, Mihajlo Kostić, Aleksandra Kezić and Marko Baralić
Metabolites 2025, 15(4), 271; https://doi.org/10.3390/metabo15040271 - 13 Apr 2025
Cited by 1 | Viewed by 1164
Abstract
Background: Chronic kidney disease (CKD) is a progressive, irreversible impairment of kidney function due to various etiologies. Numerous studies have shown that sodium-glucose cotransporter-2 inhibitors (SGLT2i) slow the progression of CKD, due to their pleiotropic effects. Therefore, there has been an increase in [...] Read more.
Background: Chronic kidney disease (CKD) is a progressive, irreversible impairment of kidney function due to various etiologies. Numerous studies have shown that sodium-glucose cotransporter-2 inhibitors (SGLT2i) slow the progression of CKD, due to their pleiotropic effects. Therefore, there has been an increase in interest in their effects not only on kidney function but also on other parameters in patients with CKD. The aim of the study was to examine the effects of SGLT2i on serum lipid values and kidney function in patients with CKD undergoing SGLT2i treatment. Methods: This study was a retrospective data analysis of 75 patients with CKD on SGLT2i treatment. We compared the values of biochemical parameters, renal function outcomes, and blood pressure at two time points: baseline and 24 months after. Results: Total cholesterol (Chol) significantly decreased in all patients, while triglyceride (Tg) and low-density lipoprotein cholesterol (LDLc) levels also decreased in all patients. High-density lipoprotein cholesterol (HDLc) levels increased, but this increase was not significant. Creatinine clearance (Ccr) significantly decreased, and serum urea (Sur) significantly increased in all patients. The proteinuria (Prt) levels did not change significantly. The results showed that the diastolic blood pressure (DBP) significantly decreased in all patients. Conclusions: This study showed that the use of SGLT2i reduced total Chol in all patients with CKD during the 24-month follow-up, regardless of diabetes mellitus (DM) status. No significant differences were observed for the Tg, LDLc, and HDLc values. Full article
(This article belongs to the Special Issue Lipid Metabolism Dysregulation in Metabolic Disorders: Unraveling the Molecular Complexity)
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