0 Glyconutrients

Background Acetaminophen overdose is a leading cause of drug-induced acute liver damage, underscoring the urgent need for accessible hepatoprotective therapies. This study evaluated the hepatoprotective effects of Aqueous Aloe vera gel extract on acetaminophen-induced liver damage in adult male Albino Wistar rats. Methodology Liver Damage was induced in Albino Wistar rats by oral administration of acetaminophen (750 mg/kg). The rats were divided into six groups: normal control, negative control, positive control (silymarin 50 mg/kg), and three treatment groups receiving Aloe vera gel extract at doses of 250 mg/kg, 500 mg/kg, and 1000 mg/kg. Body and liver weight, hematological, biochemical and oxidative stress parameters and liver histology were assessed after 7 days of treatment. Results Treatment with Aloe vera gel extract demonstrated dose-dependent hepatoprotective, anti-inflammatory and antioxidant effects with the 1000 mg/kg dose exhibiting efficacy comparable to silymarin. Higher doses (1000 mg/kg) significantly increase both the body weight and weight of the liver (p = 0.0265 and p = 0.0061); decreased the white blood cell count (p = 0.0034) and also improved hematological parameters. The extract at 1000 mg/kg also enhanced antioxidant status by reducing MDA levels (p < 0.0001) while increasing SOD (p < 0.0001) and catalase activities. Histological examination also showed that higher doses of the aqueous Aloe vera gel extract restored liver histoarchitecture, with clearly defined nuclei and cell borders. Conclusion This study demonstrates that the aqueous Aloe vera gel extract mitigates acetaminophen-induced hepatotoxicity through antioxidant, anti-inflammatory, and regenerative mechanisms. At 1000 mg/kg, it restored hepatic histoarchitecture, haematological homeostasis, normalized liver function biomarkers, and suppressed oxidative stress, rivalling silymarin in efficacy. The observed improvements in liver histology, haematological parameters, and antioxidant biomarkers indicate Aloe vera’s therapeutic potential, likely mediated through its bioactive constituents with antioxidant and anti-inflammatory properties. Further research is recommended to understand its mechanism of action, long-term and potential clinical applications.

Obesity remains a significant public health concern, with recent studies revealing that the detrimental health effects often persist even in individuals who have successfully shed excess weight. D-allulose, a low-calorie monosaccharide, has shown potential in promoting weight loss and reducing chronic inflammation associated with metabolic disorders. However, it is still unclear whether D-allulose has long-term benefits once intake is stopped. This study examined the prolonged effects of D-allulose on obesity and metaflammation. Our findings demonstrated that obese mice treated with D-allulose for one month maintained significantly lower lipid accumulation, fasting blood glucose level, glycosylated protein levels, and reduced adipose tissue inflammation compared to the Model group, even 75 days after cessation of D-allulose intake. Further cellular analyses revealed that D-allulose attenuated the activation and expression of TLR4/MyD88/NFB pathway in macrophages triggered by inflammatory stimuli. Additionally, D-allulose administration was associated with reduced protein lactylation levels in macrophages, suggesting that D-allulose may exert lasting benefits through epigenetic regulation mechanisms. These results underscore the sustained efficacy of D-allulose in combating fat accumulation, blood glucose, and inflammation, presenting a promising therapeutic approach for mitigating the residual adverse effects of obesity in individuals who have achieved weight loss.

A New Randomized Trial Says Yes. For decades, patients with atrial fibrillation (AF) have been told that caffeine is a trigger for arrhythmias. Many clinicians have reinforced this idea, urging …

Tetracycline antibiotics (TCs) are persistent pollutants that disrupt ecosystems, threaten public health, and exacerbate antimicrobial resistance in l…

Introduction Considering the shared physiological mechanisms between type 2 diabetes (T2D) and colorectal cancer (CRC), it is plausible that certain compounds may exert therapeutic effects on both diseases. Opuntia ficus-indica (nopal) has been traditionally used to manage these conditions. This study aims to elucidate the molecular mechanisms through which nopal exerts its effects on T2D and CRC. Methods Bioactive compounds of nopal, their molecular targets, and genes associated with T2D and CRC were identified from public databases. Gene Ontology (GO) analysis, metabolic pathway analysis, protein-protein interaction (PPI) network construction, and molecular docking were conducted to investigate the shared molecular targets. Results Nopal contains bioactive compounds that interact with molecular targets common to both T2D and CRC. These shared targets are implicated in lipid metabolism, apoptosis, kinase activity, interleukin-related pathways (IL-2 and IL-3), inflammation, gastrin signaling, and other critical processes. Key molecular targets identified include HSP90AA1 and MAPK8, while the principal bioactive compounds of nopal are eriodictyol and aromadendrin. Discussion The identification of eriodictyol and aromadendrin as modulators of HSP90AA1 and MAPK8 elucidates a pleiotropic mechanism underlying the link between type 2 diabetes and colorectal cancer. By modulating apoptotic and inflammatory pathways, these bioactive compounds offer a promising foundation for developing dual-action therapies targeting both metabolic and oncogenic pathways in patients with comorbid conditions. Conclusion The bioactive compounds of nopal engage multiple biological pathways relevant to T2D and CRC, suggesting that this plant may serve as a promising pharmacological candidate for the management of these diseases.

Saccharina japonica (formerly known as Laminaria japonica) is a valuable marine resource with a triple significance: it serves not only as a food sour…

The microbiota–gut–organ axis is widely recognized as a pivotal mediator of systemic health, primarily through gut-derived immune, metabolic, and inflammatory signaling. Fucoidans, a class of fucose-containing sulfated polysaccharides predominantly composed of L-fucose and exclusively found in brown seaweeds, have been demonstrated to modulate gut microbiota composition and function, resulting in the enrichment of beneficial bacteria and the suppression of harmful species. They enhance the production of beneficial metabolites, such as short-chain fatty acids and specific bile acids, while suppressing harmful metabolites, including lipopolysaccharide, thereby ameliorating organ damage via key mechanisms such as the mitigation of oxidative stress and inhibition of inflammatory responses. Furthermore, fucoidan supplementation was found to restore intestinal barrier integrity. Using disease models including Parkinson’s disease, alcoholic liver disease, diabetic kidney disease, and obesity, the mechanisms through which fucoidans ameliorate extraintestinal diseases via the microbiota–gut–organ axis were elucidated. Microbiota-dependent mechanisms have been confirmed via experimental approaches such as fecal microbiota transplantation and specific bacterial strain supplementation. Fucoidans represent promising prebiotic agents for the restoration of microbial ecology and the treatment of extraintestinal diseases, highlighting the need for further clinical investigation.

Scientific Reports - Protective role of fucoidan against cognitive deficits and redox imbalance in a scopolamine-induced Alzheimer’s disease model in rats

Background Glucosamine is a commonly used ‘over the counter’ dietary supplement. Previous research has identified an association between glucosamine use and several positive health outcomes. However, a plausible biological mechanism for these associations has not yet been identified, meaning the causality of these relationships remains unclear. A protective effect of glucosamine on the vascular endothelium has been suggested as one such possible mechanism. Albuminuria is an early marker of endothelial dysfunction within the kidney and is associated with progression of kidney disease and adverse cardiovascular outcomes. In order to provide insights into the potential biological mechanisms underlying a protective association of glucosamine use with health outcomes, we evaluated evidence for an association between glucosamine use and albuminuria in UK Biobank (N=436 200). Methods Univariable and multivariable ordinal logistic regression were performed to evaluate evidence for an association between self-reported glucosamine use and albuminuria (measured as urine albumin creatinine ratio (uACR) categories). As a secondary analysis, we performed Mendelian randomisation (MR) to demonstrate the difficulties in inferring causality in this relationship using currently available data, using summary genetic data from UK Biobank and CDKGen (N=67 452). Results We found that people who used glucosamine were more likely to be in a lower uACR group (OR 0.81, 95% CI 0.80 to 0.83, p<2.2×10−16). This association was robust to sensitivity analyses and was maintained after adjustment for age, sex and measures of obesity. In our MR analysis, we found little evidence for an association of genetically proxied glucosamine use on albuminuria (change in log uACR (mg/g) per SD change in genetic liability=1.11, 95% CI −3.01 to 5.23, p=0.60). Conclusions We found that detectable albuminuria was common in UK Biobank participants and we are the first to show that use of glucosamine supplements was associated with lower levels. Though this fits with a plausible biological role of the vascular endothelium in a potential protective effect of glucosamine use on many health outcomes, whether this relationship is causal or confounded remains unclear. We further discuss the inherent difficulties in using genetic instruments to proxy supplement use in MR analyses and highlight the need for a genome-wide association study of measured circulating glucosamine levels. Data may be obtained from a third party and are not publicly available. Data are available from the UK Biobank () for researchers who meet the criteria for access to deidentified UK Biobank data.

Lung cancer is one of the most common cancers, resulting in numerous deaths worldwide. It is classified into small-cell lung cancer and non-small cell lung cancer. The non-small cell lung cancer accounts for approximately 80% of all cases. Current chemotherapeutic treatments, often limited by severe side effects and toxicity to healthy tissues, underscore the need for more effective and better-tolerated therapies. Natural compounds, such as fucoidan, a sulfated polysaccharide extracted from brown algae, offer a promising avenue for developing such treatments due to their ability to eliminate tumor cells, delay tumor growth, and improve the effectiveness of chemotherapy drugs. Furthermore, fucoidan has received much attention in cancer therapy owing to its various advantages, including its abundance in natural sources, unique structural features of sulfate groups capable of interacting with receptors involved in cancer suppression, and its ability to modulate multiple cancer pathways. This review provides an overview of key factors contributing to lung cancer development, introduces the chemical structure and classification of fucoidans, and comprehensively examines their antilung cancer mechanisms, including apoptosis induction, proliferation inhibition, metastatic suppression, and immune modulation at the cellular level. Drug discovery and preclinical studies evaluating fucoidan in lung cancer therapy are summarized and discussed. Finally, current challenges and future research directions for fucoidan-based drug design are addressed, focusing on the steps necessary to translate promising preclinical findings into clinical applications.

Scientific Reports - Investigating fucoidan blend supplementation and resistance training in humans: a parallel randomized controlled trial design

D-allulose is a rare monosaccharide with established safety and documented biological functions, whereas its potential effects on ulcerative colitis r…

Glyphosate-Based Herbicide (GBHs) are widely used worldwide, this study investigated the ameliorative effect of Aloe Vera against GBHs hepatic toxicity in ra...

Acute kidney injury is a sudden loss of kidney function which manifests within a few hours to few days

Postprandial hyperglycemia remains a critical driver of diabetes progression. Fucoidan, a marine-derived sulfated polysaccharide with broad bioactivit…

Sarcopenia, characterized by age-related loss of muscle mass and function, presents a growing public health concern in aging populations. While resist…

The acute effect of D-allulose consumption on postprandial glycaemia and insulin secretion in healthy individuals - Volume 84 Issue OCE4

Excessive sugar intake has fueled global obesity, diabetes, and cardiovascular burdens, driving demand for natural sugar substitutes. Yet, their safet…

This study aimed to unveil the effect of glucosamine hydrochloride (GAH) and eperisone combined with exercise therapy on inflammatory markers and knee joint function in patients with knee osteoarth...

This study investigated the anti-obesity and anti-inflammatory effects of D-Allulose compared to erythritol in high-fat diet (HFD)-fed mice, focusing …

Background: Aging is associated with chronic diseases and increased oxidative stress, particularly affecting liver function. Aging is linked to chronic diseases and heightened oxidative stress, particularly impacting liver function. Recent research has demonstrated that oral administration of trehalose offers multiple benefits for various tissues and organs.Methods: This study investigated the effects of oral trehalose (2% in water) on the gene expression of key markers linked to liver oxidative stress and inflammation in 4-month-old adult and 24-month-old Wistar rats. Thirty-two male Wistar rats (n = 8) were randomly assigned into four groups: adult control, aged control, adult trehalose (2% in water), and aged trehalose, over a treatment period of one month. Following treatment, liver tissues were analyzed using real-time PCR for genes related to oxidative stress (PGC-1α, NRF2, and SOD) and inflammation (NF-κB, IL-1β, TNF-α, and TGF-β).Results: Our findings revealed a significant up-regulation of PGC-1α, NRF2, and SOD in aged trehalose group compared to the aged control (P < 0.001); however, SOD expression increased by trehalose administration in aged rats compared to other 3 groups. Inflammatory markers (NF-κB, IL-1β, TNF-α) were significantly reduced by trehalose, and TGF-β expression, involved in fibrosis, was attenuated exclusively in aged rats compared with controls (P < 0.05).Conclusion: These results suggest that trehalose has a protective effect on hepatic function, particularly in the aging population, and highlight its potential therapeutic role in age-associated liver dysfunction.

This review explores the pharmacological potential of chondroitin sulfate and fucoidan as immunomodulatory agents targeting N-acetylgalactosaminidase (nagalase) to normalize immune responses. Nagalase, an enzyme produced by tumor and virus-infected cells, contributes to immune suppression by deactivating macrophage-activating factor. Both chondroitin sulfate and fucoidan, as representatives of glycosaminoglycans and heteropolysaccharides, exhibit significant potential in inhibiting nagalase activity, thereby restoring immune functionality. Chondroitin sulfate, a key component of the extracellular matrix, demonstrates anti-inflammatory and tissue-regenerative properties by modulating nuclear factor (NF)-κB pathways and cytokine expression. Fucoidan, a sulfated polysaccharide derived from brown seaweed, enhances immune responses through macrophage and natural killer cell activation, while also exhibiting antiviral and anticancer activities. This dual action positions these compounds as promising agents for therapeutic interventions in chronic inflammatory conditions, cancer, and infectious diseases. The synergistic effects of chondroitin sulfate and fucoidan highlight their potential to address the root causes of immune dysregulation. This review aims to elucidate the underlying mechanisms of action and explore the clinical applications of these compounds within the framework of innovative immunotherapeutic strategies. However, current evidence is limited by the predominance of preclinical studies and variability in experimental models. Well-designed clinical trials are needed to validate their efficacy for therapeutic use.

This review explores the pharmacological potential of chondroitin sulfate and fucoidan as immunomodulatory agents targeting N-acetylgalactosaminidase (nagalase) to normalize immune responses. Nagalase, an enzyme produced by tumor and virus-infected cells, contributes to immune suppression by deactivating macrophage-activating factor. Both chondroitin sulfate and fucoidan, as representatives of glycosaminoglycans and heteropolysaccharides, exhibit significant potential in inhibiting nagalase activity, thereby restoring immune functionality. Chondroitin sulfate, a key component of the extracellular matrix, demonstrates anti-inflammatory and tissue-regenerative properties by modulating nuclear factor (NF)-κB pathways and cytokine expression. Fucoidan, a sulfated polysaccharide derived from brown seaweed, enhances immune responses through macrophage and natural killer cell activation, while also exhibiting antiviral and anticancer activities. This dual action positions these compounds as promising agents for therapeutic interventions in chronic inflammatory conditions, cancer, and infectious diseases. The synergistic effects of chondroitin sulfate and fucoidan highlight their potential to address the root causes of immune dysregulation. This review aims to elucidate the underlying mechanisms of action and explore the clinical applications of these compounds within the framework of innovative immunotherapeutic strategies. However, current evidence is limited by the predominance of preclinical studies and variability in experimental models. Well-designed clinical trials are needed to validate their efficacy for therapeutic use.

As the fourth-largest global food crop, the quality and functional characteristics of processed potato products are closely linked to endogenous sugar metabolism in tubers, with the trehalose–sucrose metabolism playing a key role in processing adaptability. This study analyzed 333 accessions from a tetraploid potato natural population. The trehalose and sucrose content of potato tubers at harvest was quantified using the high-performance liquid chromatography (HPLC) method. Combined with whole-genome resequencing, a genome-wide association study (GWAS) was conducted to map regulatory loci and identify candidate genes. The results showed that relative trehalose content in tubers was 20.38–24.78, while relative sucrose content was 10.32–19.50. Frequency histograms for both sugars exhibited normal distributions characteristic of quantitative traits, and a positive correlation was observed between them. GWAS for trehalose identified 111 significant SNP loci, mainly on chromosomes 10 and 12, leading to the identification of 88 candidate genes. Kyoto encyclopedia of genes and genomes analysis (KEGG) revealed that trehalose-related genes were primarily involved in pathways such as ABC transporters, tricarboxylic acid (TCA) cycle, and cysteine and methionine metabolism. Candidate genes potentially regulating tuber trehalose content included GH10, GH28, GH127, UXS, UGT, PMEI, and MYB108. For sucrose, GWAS identified 279 significant SNP loci, mainly on chromosomes 5, 6, and 12, resulting in 111 candidate genes. KEGG enrichment analysis showed that sucrose-related genes were enriched in pathways including starch and sucrose metabolism, cyanoamino acid metabolism, and phenylpropanoid biosynthesis. Candidate genes potentially regulating tuber sucrose content included GH17, GH31,GH47, GH9A4, SPP1, BGLU12, GSA1, TPS8, cwINV4, HXK, UST, MYB5, MYB14, and WRKY11. Therefore, this study provides marker loci for trehalose and sucrose metabolism research, aiming to clarify their regulatory mechanisms and support potato variety improvement and superior germplasm development.

Regular use of glucosamine was associated with a reduced risk of several age-related chronic diseases. Further studies are needed to confirm these findings and to clarify its potential role in supporting healthy aging.

This study aimed to elucidate the anticancer mechanism of Fucoidan (FCD) in Benzo(a)pyrene (B(a)P)-induced lung cancer, especially its effect on club …

Rheumatoid arthritis is a persistent immune-mediated inflammatory disorder that primarily affects joint bones, impacting approximately 0.5–1.0% of the global population. People with RA are 1.5 times more likely to develop cardiovascular conditions, including atherosclerosis. This study explored the therapeutic potential of GAc in a rat model of RA induced by CFA, focusing on its impact on biomarkers associated with atherosclerosis. Molecular docking studies indicated strong binding affinities of GAc with key inflammatory cytokines, including TNF-α, IL-6, IL-1β, NF-κB and PRMT-1. The experimental model of 23 days involved the induction of arthritis by injecting 0.15 mL of CFA into the sub-plantar region of the rats’ left hind paws. GAc was dissolved in distilled water and administered to rats via oral gavage. Our results revealed that the administration of GAc, particularly in combination with MtxSt (GAc 10 g/kg + MtxSt), significantly (p < 0.001) reduced arthritic scores, joint stiffness scores, paw thickness, levels of lipids (LDL, VLDL, TG, and TC), asymmetric dimethylarginine (ADMA), homocysteine, oxidative stress, and pro-inflammatory cytokines. In addition, GAc markedly (p < 0.001) improved body weight, hematological parameters (RBC, %HCT and Hb), HDL, dimethylarginine dimethylaminohydrolase-1(DDAH-1), and CST levels. Histopathological assessments showed that GAc 10 g/kg + MtxSt significantly alleviated bone and cartilage erosion (p < 0.001), pannus formation (p < 0.001), synovial hyperplasia (p < 0.01), vascular congestion (p < 0.001) and inflammatory cell infiltration (p < 0.001). The therapeutic efficacy of GAc is ascribed to its anti-inflammatory, antioxidant, and anti-atherosclerotic properties. This study suggested that combining GAc with MtxSt exerts a synergistic effect in mitigating inflammation and reducing the risk of atherosclerosis associated with RA.

This study clarified the structure and digestive properties of the Laminaria japonica polysaccharide (LJP). It was demonstrated that LJP belongs to a heteropolysaccharide composed of mannuronic acid, fucose, galactose, glucuronic acid, mannose, xylose, glucose, and guluronic acid in the proportion of 34.56%: 30.55%: 10.63%: 7.52%: 6.66%: 3.74%: 3.62%: 2.72%, with a backbone chain composed of →4)-β-d-ManA-(1→, →3)-α-l-Fucp-(1→, →4)-α-GulA-(1→, →3,4)-α-GlcA-(1→, and →4)-β-d-GlcA-(1→. In vivo fluorescence imaging indicated that LJP was mainly distributed in the stomach and intestinal segments of mice, and the fluorescence signal gradually disappeared after 12 h of digestion. In addition, LJP had no effect on the phenotype and general health of mice while promoting the proliferation of the beneficial bacteria Rikenella, Rikenellaceae_RC9_gut_group. Notably, 100 mg/kg LJP significantly increased the levels of acetic and butyric acid in the mice feces, which were 1.51 and 2.65 folds higher than the controls, respectively. Our study illuminated the absorption and distribution mechanism of LJP, providing a scientific reference for revealing LJP as a potential prebiotic.