Glycosylation, the enzymatic addition of glycans to proteins and lipids, is a critical post-translational modification that influences protein folding, stability, trafficking, immune modulation, and cell signaling. The vast structural diversity of glycans arising from differences in monosaccharide composition, branching, and terminal modifications such as sialylation, fucosylation, and sulfation underpins their functional specificity and regulatory capacity. This review provides a comprehensive overview of glycan biosynthesis, with a focus on N-glycans, O-glycans, glycosaminoglycans (GAGs), and glycolipids. It explores their essential roles in maintaining cellular homeostasis, development, and immune surveillance. In health, glycans mediate cell–cell communication, protein interactions, and immune responses. In disease, however, aberrant glycosylation is increasingly recognized as a hallmark of numerous pathological conditions, including cancer, neurodegenerative disorders, autoimmune diseases, and a wide range of infectious diseases. Glycomic alterations contribute to tumor progression, immune evasion, therapy resistance, neuroinflammation, and synaptic dysfunction. Tumor-associated carbohydrate antigens (TACAs) and disease-specific glycoforms present novel opportunities for biomarker discovery and therapeutic targeting. Moreover, glycan-mediated host–pathogen interactions are central to microbial adhesion, immune escape, and virulence. This review highlights current advances in glycomics technologies, including mass spectrometry, lectin microarrays, and glycoengineering, which have enabled the high-resolution profiling of the glycome. It also highlights the emerging potential of single-cell glycomics and multi-omics integration in precision medicine. Understanding glycome and its dynamic regulation is essential for uncovering the molecular mechanisms of disease and translating glycomic insights into innovative diagnostic and therapeutic strategies.

Xylooligosaccharides derived from Xylan, significant component of hemicellulose in lignocellulosic plant biomass, are essential raw materials used in the food, pharmaceutical and agricultural industries. They find application in these industries due to their unique physicochemical properties such as pH stability, growth regulatory ability, and anti-allergic property. In addition, they have been shown to exhibit promising antimicrobial, anti-cancer, antioxidant and anti-inflammatory activities. Xylooligosaccharides convert waste into valuable foods, pharmaceuticals, and agricultural products, promoting health, the economy, and the environment.

Clinical studies have linked glyphosate exposure to substantial morbidity, with acute kidney injury occurring in some cases. Although the toxic effects of glyphosate-based herbicides (GBHs) have been reported in several studies, their molecular impact on renal function remains poorly understood. Given the kidney’s critical role in excretion, it is particularly susceptible to damage from xenobiotic exposure. In this study, we aim to identify N-glycomics and proteomics change in the kidney following chronic GBH exposure, to better understand the mechanisms behind glyphosate-induced kidney damage. Kidney tissues from female and male rats were analyzed using liquid chromatography–tandem mass spectrometry. The results revealed notable changes in the N-glycan composition, particularly in the fucosylated and sialofucosylated N-glycan types. The proteomic analysis revealed the activation of immune signaling and inflammatory pathways, including neutrophil degranulation, integrin signaling, and MHC class I antigen presentation. Transcription regulators, such as IL-6, STAT3, and NFE2L2, were upregulated, indicating a coordinated inflammatory and oxidative stress response. Sex-specific differences were apparent, with female rats exhibiting more pronounced alterations in both the N-glycan and protein expression profiles, suggesting a higher susceptibility to GBH-induced nephrotoxicity. These findings provide new evidence that chronic GBH exposure may trigger immune activation, inflammation, and potentially carcinogenic processes in the kidney.

Eating behavior requires a balance between metabolic and hedonic components. Anxiety and dietary type may influence the quantity, patterns, and other aspects of food intake. Modern diets, especially in Western societies, often contain high levels of calories from fat and simple sugars (e.g., cafeteria-style diets). This type of diet may promote overweight and/or obesity in some, although many consumers remain at a normal weight. The mechanisms underlying susceptibility or resistance to weight gain remain unclear. Here, Sprague-Dawley male rats were fed a cafeteria diet for 10 weeks and then classified into quartiles based on body mass. We evaluated locomotor activity and anxiety-like behaviors and analyzed hypothalamic proteomics in overweight (Q4) rats compared with underweight (Q1) rats. Our results showed that locomotor activity and anxiety-like behaviors did not differ across quartiles (p > 0.05). Nevertheless, the expression of several hypothalamic proteins differed between Q4 and Q1 rats. Functional enrichment analysis of these differentially expressed proteins (p ≤ 0.05) revealed changes in cytoskeleton dynamics, synaptic communication, energy production and utilization, biosynthesis of cellular components (including nucleotides and carbohydrates), and regulation of metabolism between Q1 and Q4 rats. Neuro-humoral hypothalamic output regulates metabolism and food intake. Therefore, these functional changes in the hypothalamus may be associated with rats’ susceptibility/resistance to weight gain.

Organophosphate pesticides (OPPs) are widely used in agriculture and are associated with metabolic dysregulation and cognitive impairment. Emerging evidence links OPP exposure to insulin resistance and diabetes mellitus, a condition known to negatively impact brain function. Prior investigations in our laboratory identified significant dysregulation of arachidonic acid (AA) metabolites associated with the endocannabinoid system in both diabetic patients and those with chronic OPP exposure, with a marked reduction in serum AA levels in the OPP-exposed cohort. This study investigates the impact of OPP exposure and pre-diabetes on the hippocampal proteome and whether AA supplementation can mitigate the resulting neuronal proteomic alterations. Using a controlled rat model, high-resolution LC-MS/MS-based proteomics identified differentially expressed proteins across experimental groups. Both OPP exposure and pre-diabetes were associated with increased cognitive impairment and were associated with overlapping disruptions in pathways related to insulin resistance, mitochondrial function, synaptic plasticity, and neuronal development. AA supplementation mitigated cognitive decline and stabilized synaptic and metabolic proteins; however, residual pathway dysregulation highlights the complexity of these stressors. Our results reveal novel molecular intersections between environmental and metabolic drivers of cognitive impairment, establishing a rationale for further research into inexpensive, protective dietary interventions.

Cafeteria diet, rich in fat and sugar, rapidly induces metabolic dysfunction and alters central energy regulation. We examined behavior and hypothalamic protein abundance profiles in cafeteria-diet-fed rats classified into weight-gain quartiles (Q1–Q4) and compared with standard-chow-fed controls. Pre-adolescent male Sprague–Dawley rats (n = 39:10 controls; Q1–Q4, n = 7–8 each) received ad libitum access to standard chow or a palatable cafeteria diet and underwent open field testing followed by quantitative LC–MS/MS proteomics of the hypothalamus. Behavioral assessment showed no major differences in locomotion, anxiety-like parameters, or exploration, except for reduced grooming (p ≤ 0.05) in cafeteria-fed versus control animals. Global, threshold-independent analyses showed that the lower-weight-gain phenotype (Q1) was significantly more distant from controls than the higher-weight-gain phenotype (Q4) (multivariate distance to the control centroid; Mann–Whitney U, p = 0.006), a pattern also observed by principal component analysis and hierarchical clustering. Consistently, of 17 proteins that remained significant after false discovery rate correction, 16 differed between Q1 and control and only one between Q4 and control, despite both phenotypes having ad libitum access to the same cafeteria diet. These findings suggest that lower weight gain is associated with more extensive hypothalamic protein abundance changes, although a causal link remains to be established, and they highlight candidate pathways for future mechanistic studies.