Glycolysis, present in most organisms, is evolutionarily one of the oldest metabolic pathways. It has great relevance at a physiological level because it is responsible for generating ATP in the cell through the conversion of glucose into pyruvate and reducing nicotinamide adenine dinucleotide (NADH) (that may be fed into the electron chain in the mitochondria to produce additional ATP by oxidative phosphorylation), as well as for producing intermediates that can serve as substrates for other metabolic processes. Glycolysis takes place through 10 consecutive chemical reactions, each of which is catalysed by a specific enzyme. Although energy transduction by glucose metabolism is the main function of this pathway, involvement in virulence, growth, pathogen–host interactions, immunomodulation and adaptation to environmental conditions are other functions attributed to this metabolic pathway. In humans, where glycolysis occurs mainly in the cytosol, the mislocalization of some glycolytic enzymes in various other subcellular locations, as well as alterations in their expression and regulation, has been associated with the development and progression of various diseases. In this review, we describe the role of glycolytic enzymes in the pathogenesis of diseases of clinical interest. In addition, the potential role of these enzymes as targets for drug development and their potential for use as diagnostic and prognostic markers of some pathologies are also discussed.

Revista Colombiana de Biotecnología de la Universidad Nacional de Colombia

In this work, the main approaches for the preparation of encapsulating matrices using chitosan-containing formulations have been reviewed. Various methodologies have been considered, such as physical intermolecular bonds and chemical crosslinking reactions, including the click reactions which have become novel in the cross-linking of systems containing this biopolymer. Likewise, the formation of different macroscopic assemblies such as spheroids, vesicles, layer by layerpolycomplexes, etc., has been addressed. In the final part of the work, the main achievements reported with these matrices in the encapsulation of cells, both eukaryotic and prokaryotic, are discussed, emphasizing their potential applications and perspectives in different fields as medicine (treatment of traumatic diseases, diabetes, venous diseases, tissue regeneration, transplantation and tolerance); food (administration of probiotics); industrial applications (bioethanol production); etc.

Methods: We quantified the expression levels of four miRNAs (hsa-miR-128-3p, hsa-miR-21-3p, hsa-miR-223-3p, and hsa-let-7a) in liver samples obtained during bariatric metabolic surgery from patients with obesity and healthy controls using qPCR. Expression was normalized to hsa-miR-24-3p, selected as the most stable reference gene in our cohort. Associations between miRNA levels and clinical or demographic variables (sex, AMPs) were also explored. Results: Compared with controls, patients with obesity showed significant dysregulation of hsa-miR-128-3p and hsa-miR-223-3p, independent of histological liver alterations. No consistent changes were observed for hsa-miR-21-3p or hsa-let-7a. Clinical variables, including AMPs, did not account for the observed differences. Conclusion: miR-128-3p and miR-223-3p are linked to obesity-related metabolic dysfunction and emerge as promising biomarkers or therapeutic targets.

Glycolysis is primarily involved in ATP production but also modulates oxidative stress. Chronic alcohol consumption is correlated with an increased incidence of multiple diseases, including cancer and neurodegenerative diseases (NDDs), though the underlying mechanisms remain unclear. Guided by a literature review and bioinformatics analysis, we evaluated the expression of 22 genes encoding various isoforms of seven glycolytic enzymes (GEs) in the peripheral blood of patients with alcohol use disorder (AUD), individuals with acute alcohol consumption (AAC), and their respective control groups using qPCR. In parallel, we evaluated the expression of selected genes coding for GEs linked to NDDs, as well as astrocytic markers in primary mouse astrocyte cultures exposed to ethanol. Thirteen GE-related genes, including non-canonical isoforms, were significantly dysregulated in AUD patients; notably, eight of these genes showed similar alterations in individuals with AAC. Several enzymes encoded by these genes are known to be regulated by oxidative stress. Ethanol-exposed astrocytes also showed altered expression of glycolytic genes associated with NDDs and astrocyte function. These findings indicate that glycolytic dysregulation is driven by ethanol intake, regardless of exposure duration or organic damage, highlighting a link between ethanol-driven redox imbalance and glycolytic remodeling, which could contribute to organ damage.

Alcohol use disorder (AUD) is influenced by genetic factors that affect key neurobiological systems, including dopaminergic and GABAergic pathways, which regulate neurobehavioral functions and are modulated by brain-derived neurotrophic factor (BDNF). Variations in these genes contribute to individual vulnerability to AUD. In this study, we investigated single-nucleotide polymorphisms (SNPs) and haplotypic associations in GABRA1, GABRA2, and GABRA6, along with the dopaminergic pathway genes DRD2/ANKK1 and BDNF, in a Spanish cohort. Peripheral blood-derived genomic DNA was genotyped, and haplotype analyses were conducted. Individual SNPs in GABRA1, GABRA2, BDNF, and DRD2/ANKK1 showed no significant associations with AUD. In GABRA6, the rs3219151 T allele was more frequent in AUD patients than in controls (57.9% vs. 49.3%; p = 0.03), while the C allele appeared to show a potential protective association. In addition, the GAC haplotype of GABRA6 (rs2197414, rs1992647, rs3219151) was less frequent in AUD than in controls (0.071 vs. 0.122) and showed a protective association (OR = 0.58; 95% CI = 0.34–0.99; p = 0.045). Our findings provide exploratory evidence suggesting that specific genetic variants and haplotypes may contribute to AUD susceptibility and support the relevance of multigenic and haplotypic approaches for exploring the neurobiological mechanisms underlying AUD.