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Metabolites
Special Issues
Metabolic Profiling in Neurometabolisms
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Metabolic Profiling in Neurometabolisms

A special issue of Metabolites (ISSN 2218-1989).

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

Special Issue Editor

Dr. Larissa Daniele Bobermin

E-Mail Website
Guest Editor
Department of Biochemistry, Federal University of Rio Grande do Sul, Porto Alegre 90035-003, Brazil
Interests: neural cell culture; astroglial functionality and metabolism; neurotoxicity; neuroprotective molecules

Special Issue Information

Dear Colleagues,

The metabolism within the brain, or neurometabolism, encompasses high-complexity metabolic pathways and networks. The energy demand can vary throughout the brain depending on region, degree of activity, and cell type, and is mainly supplied by glucose. In addition to meeting cellular ATP demands, pathways related to glucose, lipid, and amino acid metabolism provide key metabolites to brain activity, including neurotransmitters and other intercellular communication factors, reducing power for biosynthetic and antioxidant pathways, and other molecules that participate in maintaining brain structural and functional integrity. The field of neurometabolism also involves the central control of the body’s energy homeostasis and feeding behavior, which are importantly regulated by the hypothalamus. Not surprisingly, brain metabolic abnormalities and disorders are associated with a wide range of pathological conditions that affect the developing, adult, and aging brain.

This Special Issue of Metabolites aims to cover a broad range of themes addressing brain energy supply and its regulation; genetic, biological (age, gut microbiota, inflammation, oxidative stress), and environmental (nutrition, lifestyle, stress) factors that modulate neurometabolism; cellular metabolic particularities and how they shape brain functions; the role of glial cells in neurometabolism and neuron–glial metabolic cooperations; subcellular/organellar and biochemical processes that lead to damage or dysfunction of neural cells; neurometabolic imaging; peripheral-to-brain crosstalk and how brain influences systemic metabolism; metabolic interventions focusing on neuroprotection and therapeutic opportunities. Other topics regarding brain metabolic profiles in health and disease are also welcome. This Special Issue is not only intended for preclinical results (in vitro and animal models) but is also open to clinical studies, new methods, and review articles.

Dr. Larissa Daniele Bobermin
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 250 words) can be sent to the Editorial Office for assessment.

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

  • brain
  • energy homeostasis
  • glial cells
  • metabolic disorders
  • metabolic profiles
  • neurometabolism
  • neurons

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Published Papers (3 papers)

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Research

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15 pages, 1439 KB  
Article
Resveratrol Mitigates High Glucose-Induced Inflammation in Astroglial Cells
by Vanessa Sovrani, Filipe Renato Pereira Dias, Rômulo Rodrigo de Souza Almeida, Krista Minéia Wartchow, Nícolas Manzke Glänzel, Ester Rezena, Carlos-Alberto Gonçalves, Guilhian Leipnitz, Larissa Daniele Bobermin and André Quincozes-Santos
Metabolites 2025, 15(12), 771; https://doi.org/10.3390/metabo15120771 - 28 Nov 2025
Viewed by 286
Abstract
Background/Objectives: Changes in glucose metabolism impact central nervous system (CNS) homeostasis and, consequently, can lead to cognitive impairment and an increased risk for neurodegenerative and neuropsychiatric disorders. Astrocytes are glial cells that act as key regulators of brain glucose metabolism, thus representing important [...] Read more.
Background/Objectives: Changes in glucose metabolism impact central nervous system (CNS) homeostasis and, consequently, can lead to cognitive impairment and an increased risk for neurodegenerative and neuropsychiatric disorders. Astrocytes are glial cells that act as key regulators of brain glucose metabolism, thus representing important cellular targets for studies of different pathophysiological conditions, including hyperglycemia. Resveratrol, a natural polyphenol, has emerged as a potential protective strategy against diabetes and its complications; however, its glioprotective effects remain unclear. Based on these observations, we evaluated whether resveratrol could modify the inflammatory response in astroglial cells exposed to experimental hyperglycemic conditions. Methods: After reaching confluence, C6 astroglial cells were pre-incubated with 10 µM resveratrol in serum-free DMEM with 6 mM glucose for 24 h. The medium was then replaced with serum-free DMEM containing 12 mM glucose and 10 µM resveratrol for another 24 h. Controls were maintained in 6 mM glucose. Analyses included cell viability, metabolic activity, glucose and glutamate uptake, cytokine quantification by ELISA, and gene expression by RT-qPCR. Results: We show that high glucose levels modulate glucose and glutamate metabolism, and increase neuroinflammation, through the modulation of inflammatory mediators. In addition, high glucose upregulated the gene expressions of inducible nitric oxide synthase (iNOS), nuclear factor κB (NFκB), cyclooxygenase 2 (COX2), and Toll-like receptor 4 (TLR4) while decreasing mRNA levels of NLR family pyrin domain containing 3 (NLRP3) and peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α). However, resveratrol was able to prevent most of these effects, particularly the high glucose-triggered inflammatory response. Resveratrol also modulated heme oxygenase 1 (HO-1) and nuclear factor erythroid-derived 2-like 2 (Nrf2), important targets associated with cellular protection. Conclusions: Our findings reinforce resveratrol as a potential glioprotective strategy against diabetes-related brain toxicity. Full article
(This article belongs to the Special Issue Metabolic Profiling in Neurometabolisms)
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13 pages, 1451 KB  
Article
Glutamine and Albumin Levels in Cerebrospinal Fluid Are Correlated with Neurological Severity in an Experimental Model of Acute Hepatic Encephalopathy
by Pedro Arend Guazzelli, Felipe dos Santos Fachim, Anderson Santos Travassos, Caroline Casagrande Schaukoski, Pâmela Cristina Lukasewicz Ferreira, Fernanda Uruth Fontella, Marco Antônio de Bastiani, Adriano Martimbianco de Assis and Diogo Onofre Souza
Metabolites 2025, 15(9), 598; https://doi.org/10.3390/metabo15090598 - 8 Sep 2025
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Abstract
Background/Objectives: Hepatic encephalopathy (HE) is a severe neurological complication of acute liver failure (ALF) characterized by the accumulation of neurotoxic metabolites and impaired cerebral function. We aimed to examine the correlation between HE severity and cerebrospinal fluid (CSF) biomarker levels in a rat [...] Read more.
Background/Objectives: Hepatic encephalopathy (HE) is a severe neurological complication of acute liver failure (ALF) characterized by the accumulation of neurotoxic metabolites and impaired cerebral function. We aimed to examine the correlation between HE severity and cerebrospinal fluid (CSF) biomarker levels in a rat model of ALF induced by subtotal hepatectomy. Methods: Male Wistar rats underwent 92% hepatectomy and were monitored for neurological impairment via a standardized HE score. At twenty-four hours post surgery, CSF and blood were collected for biochemical analysis. Results: We found a significant positive correlation between neurological severity and CSF levels of glutamine (r = 0.929, p < 0.001) and albumin (r = 0.869, p < 0.001), both with HE grade I scores, highlighting their prominent role as HE biomarkers. Other amino acids, including aspartate (r = 0.790, p < 0.001), glutamate (r = 0.853, p < 0.001), isoleucine (r = 0.834, p < 0.001), leucine (r = 0.813, p < 0.001), lysine (r = 0.861, p < 0.001), methionine (r = 0.889, p < 0.001), phenylalanine (r = 0.916, p < 0.001), ornithine (r = 0.775, p < 0.001), tryptophan (r = 0.814, p < 0.001), and valine (r = 0.721, p < 0.001), also showed significant correlations with HE severity but not with HE grade I scores. Conclusions: These findings underscore the potential of glutamine and albumin in CSF as key biomarkers for assessing neurological severity in ALF patients. Full article
(This article belongs to the Special Issue Metabolic Profiling in Neurometabolisms)
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Review

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13 pages, 640 KB  
Review
Methylglyoxal, a Knot to Be Untied in Brain Glucose Hypometabolism
by Vitor Gayger-Dias, Vanessa-Fernanda Da Silva, Thomas Michel Sobottka, Marina Concli Leite, Adriana Fernanda K. Vizuete and Carlos-Alberto Gonçalves
Metabolites 2025, 15(11), 690; https://doi.org/10.3390/metabo15110690 - 24 Oct 2025
Viewed by 551
Abstract
Background: Advanced glycation end products (AGEs) and receptors for AGEs (RAGE) have been extensively implicated in metabolic and neurodegenerative disorders due to their capacity to alter protein structure and function through non-enzymatic glycation. More recently, methylglyoxal (MG), a highly reactive glycolytic byproduct, has [...] Read more.
Background: Advanced glycation end products (AGEs) and receptors for AGEs (RAGE) have been extensively implicated in metabolic and neurodegenerative disorders due to their capacity to alter protein structure and function through non-enzymatic glycation. More recently, methylglyoxal (MG), a highly reactive glycolytic byproduct, has gained attention as a critical mediator of AGE formation and an independent contributor to cellular distress, particularly in the context of diabetes mellitus and Alzheimer’s disease. Objectives: This review synthesizes evidence from experimental and clinical studies addressing MG generation and metabolism in brain tissue, emphasizing the glyoxalase system as the primary detoxification mechanism, the functional contribution of astrocytes, and the downstream consequences of MG accumulation. In addition, we examined the interplay between MG, RAGE signaling, unfolded protein response, and regulatory mechanisms involving the hexosamine biosynthesis pathway and O-GlcNAcylation of key proteins in glucose metabolism and insulin signaling. Results and Conclusions: Brain glucose hypometabolism is a consequence of insulin resistance and results in a metabolic rearrangement that expands the glycolytic pathway and generates more MG, which, in turn, can affect insulin signaling, further compromising the molecular basis of insulin resistance and creating a vicious cycle. Astrocytes are key cells in the generation and detoxification of MG in the brain, making them a therapeutic target. Full article
(This article belongs to the Special Issue Metabolic Profiling in Neurometabolisms)
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