Search Results (39)

Malnutrition, sarcopenia, and frailty are highly prevalent in patients with chronic liver disease and are closely associated with poor clinical outcomes. This review highlights the complex interplay between macronutrient metabolism and muscle wasting in liver cirrhosis. We explore the alterations in glucose, lipid, and amino acid metabolism that occur in cirrhosis, including the role of skeletal muscle in compensatory ammonia detoxification. The review also discusses the emerging evidence on sarcopenia as a prognostic marker and therapeutic target, with a focus on the role of branched-chain amino acid (BCAA) supplementation. While several studies have demonstrated the clinical benefits of BCAA in improving muscle mass, hepatic encephalopathy, and quality of life, results remain mixed, emphasizing the need for further well-designed clinical trials. Understanding the muscle–liver–gut axis may offer novel insights into therapeutic strategies for managing sarcopenia in liver disease. Full article

Dietary nutrients are crucial for human health and the survival of gut microbes. Diet plays a central role in gut microbiota, as microbes rely on ingested nutrients for biological functions. Research highlights the connection between gut microbiota and exercise. Moderate and intense exercise are common in endurance training. Studies suggest gut microbiota may influence athlete health and performance. Athletes should consider dietary strategies like protein supplements, carbohydrate loading, probiotics, and prebiotics. The diverse gut microbiome of elite athletes produces key metabolites like short-chain fatty acids. A gut–muscle axis may exist, influencing muscle quality and gut biodiversity. This work summarizes current knowledge on diet, exercise, gut microbiota, and skeletal muscle. Full article

Cancer cachexia is a multifactorial syndrome characterized by metabolic dysregulation, inflammation, and progressive loss of skeletal muscle mass. Frequently observed in colorectal cancer patients, it is associated with poor clinical outcomes and reduced treatment tolerance. Current therapies provide limited benefit, underscoring the need for integrative approaches. Grape seed polyphenols, particularly oligomeric proanthocyanidins, have demonstrated potential to modulate catabolic signaling, mitochondrial dysfunction, and inflammatory responses involved in cachexia pathophysiology. This review integrates preclinical and clinical evidence on the use of grape seed-derived products, highlighting their effects on NF-κB and AMPK pathways, redox homeostasis, and gut–muscle axis. Furthermore, the nutritional composition and bioactive properties of grape seed flour—rich in fiber and phenolic compounds—are discussed in the context of nutraceutical applications. A clinical trial currently underway in Brazil aims to evaluate the effects of grape seed flour supplementation in colorectal cancer patients with cachexia. Altogether, grape-derived compounds offer a safe, low-cost, and mechanistically grounded strategy for improving nutritional status and resilience in oncological care. Full article

Sarcopenia, the age-related loss of skeletal muscle mass and function, is associated with inflammation, mitochondrial dysfunction, and gut barrier impairment. This study investigates the postbiotic effects of heat-killed Lactiplantibacillus plantarum HY7715 (HY7715) and its extracellular vesicles (EVs) on muscle health and intestinal integrity. In C2C12 myotubes, both treatments enhanced myogenic differentiation by upregulating Myf5 and MYOG, and improved mitochondrial activity and biogenesis via increased PGC1α and mTOR expression. Under TNFα-induced muscle atrophy, they suppressed expression of atrophy-related markers (Fbox32, MuRF1, and myostatin). EVs showed stronger anti-inflammatory effects by reducing IL6 expression in muscle cells. In intestinal Caco-2 cells, HY7715-derived EVs improved barrier function by upregulating tight junction proteins (ZO-1, occludin, and claudins), and effectively reduced LPS-induced inflammation. These findings suggest that heat-killed HY7715 and its EVs may alleviate sarcopenia by enhancing muscle regeneration and maintaining intestinal homeostasis, highlighting their potential as safe, gut–muscle axis-targeting postbiotic interventions for healthy aging. Full article

Background: Traditional fermented soybean foods, acting as potential synbiotics, may help mitigate cognitive impairment associated with amnesia. This study investigated the neuroprotective effects of four kanjang (Korean fermented soy sauce) varieties and their underlying mechanisms. Methods: Male Sprague Dawley rats (n = 70) were divided into seven groups: normal control, scopolamine control, positive control (1 mg/kg bw/day of donepezil), and four scopolamine-treated groups receiving different kanjang varieties (0.5% in high-fat diet). Based on their Bacillus content, the kanjang samples were categorized as traditionally made kanjang (TMK) with high Bacillus (SS-HB), TMK with medium Bacillus (SS-MB), TMK with low Bacillus (SS-LB), and factory-made kanjang (SS-FM). Results: Scopolamine administration disrupted energy, glucose, and water metabolism and impaired memory function (p < 0.05). All kanjang treatments improved insulin sensitivity, reduced inflammation, enhanced glucose tolerance, and decreased visceral fat. SS-MB, SS-HB, and SS-FM increased skeletal muscle mass. They maintained body water homeostasis by suppressing the renin–angiotensin–aldosterone system. Kanjang treatments improved memory function, with SS-FM showing the least significant effects. The treatments reduced neuronal cell death in the hippocampal CA1 region, decreased acetylcholinesterase activity, and increased brain-derived neurotrophic factor mRNA expression. Gut microbiota analysis revealed that kanjang treatments increased Lactobacillaceae and decreased Lachnospiraceae, with SS-HB and SS-LB specifically elevating Ligilactobacillus. Metagenomic analysis demonstrated enhanced glycolysis/gluconeogenesis pathways and enhanced butanoate metabolism while reducing lipopolysaccharide biosynthesis and pro-inflammatory signaling. SS-MB and SS-LB increased intestinal goblet cell counts and the serum butyrate concentration. Conclusions: These findings suggest that kanjang consumption, particularly SS-HB and SS-LB varieties, can ameliorate memory impairment in this murine model through multiple mechanisms: metabolic improvements, enhanced neurotrophic signaling, gut microbiota modulation, and reduced neuroinflammation via gut–brain axis activation. Human clinical trials are warranted to determine if these promising neuroprotective effects translate to clinical applications. Full article

Background/Objectives: Recent studies have highlighted the role of the gut–muscle axis, suggesting that modulation of the gut microbiota may indirectly benefit skeletal muscle. This study aimed to evaluate the effects of Lactobacillus fermentum (L. fermentum) supplementation in a model of muscle atrophy induced by chronic ethanol (EtOH) intake, focusing on inflammatory and antioxidant mechanisms. Methods: Sixty 12-month-old female Balb/c mice were divided randomly into three groups (n = 20/group): (1) Ethanol (EtOH) group, receiving ethanol daily for 8 and 12 weeks to induce systemic oxidative stress and inflammation; (2) Ethanol + Probiotic (EtOH + P) group, receiving both ethanol and L. fermentum supplementation for the same durations; and (3) Control (Ctrl) group, receiving only water. Muscle samples were analyzed for the fiber morphology, inflammatory markers, oxidative stress indicators, and satellite cell (SC) activity. All data were tested for normality using the Shapiro–Wilk test before applying a parametric analysis. A statistical analysis was performed using one-way ANOVA followed by a Bonferroni post-hoc test. The level of significance was set at p < 0.05. Results: EtOH exposure caused significant atrophy in all muscle fiber types (type I, IIa, and IIb), with the most pronounced effects on oxidative fibers. L. fermentum supplementation significantly reversed atrophy in type I and IIa fibers, accompanied by a significant reduction in IL-6, TNF-α, and Hsp60 expression levels, indicating the protective effect of L. fermentum against oxidative stress and inflammation. Moreover, the probiotic treatment increased MyoD expression in SCs, suggesting enhanced regenerative activity, without histological evidence of fibrosis. Conclusions: These findings suggest that L. fermentum supplementation could counteract EtOH-induced skeletal muscle damage by reducing inflammation and oxidative stress and promoting muscle repair, indicating its potential as an adjuvant, in the therapeutic strategy of models of muscle degeneration. Full article

Public concern over drug resistance has led to governmental regulations banning the use of antibiotics as growth promoters, stimulating interest in developing complementary strategies to maintain animal production, mitigate infections, and enhance muscle characteristics and quality parameters, especially in meat-producing animals. Probiotics are recognized as a potential strategy for improving growth, primarily by promoting intestinal homeostasis. These microorganisms are suggested to modulate gut microbiota, preserving their ecosystem and influencing secondary metabolite production, which can directly or indirectly regulate skeletal muscle metabolism by influencing the expression of key muscle-related genes and the activity of various signaling factors. Several studies have documented the potential benefits of various strains of Bacillus, Enterococcus, and members of the Lactobacillaceae family on muscle characteristics. These studies have shown that probiotics not only modulated myogenic factors but also influenced proteins and enzymes involved in signaling pathways related to carbon metabolism, inflammatory response, mitochondrial dynamics, and antioxidant activity. These effects have been associated with improvements in meat quality parameters and enhanced growth performance. This manuscript seeks to present a brief overview of the impact of probiotic supplementation on muscle health and the quality of meat in broiler chickens. Full article

There has been a growing interest globally in vegan and vegetarian diets over the last decade for a combination of health, ethical, environmental, spiritual, and social reasons. In line with this popularity, research examining the role of plant-based food sources, including vegan and vegetarian diets, in supporting skeletal muscle remodeling and anabolism in humans has also received considerable attention. The emergence of the microbiota-gut–muscle axis, a bidirectional pathway where the gut microbiota impacts skeletal muscle and vice versa, has been suggested as a potential mediator of food and nutrition’s influence on the mechanistic processes that regulate muscle mass and function. Considering inherent nutritional differences between vegan, vegetarian, and omnivorous diets related to the fiber and macronutrient content, presence of anti-nutritional factors, and diverse food and supplemental sources for obtaining protein, it stands to reason that the regulation of the microbiota–gut–muscle axis via diet-induced changes in gut microbiota composition and function may be dissimilar. However, whether this translates into differential effects on the skeletal muscle is unclear. This review article aims to provide a contemporary perspective for how variations in gut microbiota linked to vegan, vegetarian, and omnivorous diets may be a potential mechanism for influencing protein metabolism in skeletal muscle mass via a purported microbiota-gut–muscle axis. Full article

Background/Objectives: Sarcopenia is characterized by loss of muscle mass and strength and is associated with aging. Recently, its links with the gut–muscle axis have been reported, suggesting that probiotics could influence muscle health. Methods: In the present study, we investigated the protective roles of two lactic acid bacteria strains, Streptococcus salivarius subsp. thermophilus ST-G30 (ST-G30) and Lacticaseibacillus paracasei LPc-G110 (LPc-G110), on skeletal muscle atrophy induced by dexamethasone (DEX) in C2C12 myotubes. Results: Our results demonstrated that ST-G30 significantly alleviated DEX-induced myotube atrophy by increasing the myotubes’ diameter (25.95 ± 1.28 vs. 15.30 ± 0.30 μm, p < 0.01), improving the fusion index (48.35 ± 1.75 vs. 22.16 ± 2.36%, p < 0.0001), and increasing the protein content (1.78 ± 0.02 vs. 1.56 ± 0.01 mg/mL, p < 0.05) and myotube length (0.61 ± 0.05 vs. 0.33 ± 0.01, p < 0.05), whereas LPc-G110 showed no significant effect on these phenotypes (p > 0.05). Transcriptomic analysis reveals that ST-G30 modulates critical signaling pathways and biological processes related to skeletal muscle health. In the current study, KEGG enrichment analysis and WGCNA enabled identification of the PI3K-Akt signaling pathway as a key regulator of these processes, highlighting its essential role in mitigating DEX-induced muscle atrophy. Furthermore, the overlapping DEGs associated with the PI3K-Akt signaling pathway showed strong correlations with muscle atrophy-related indices. Conclusions: These findings underscore the potential of ST-G30 as a promising anti-muscle atrophy supplement and provide valuable insights for developing strategies to prevent and treat glucocorticoid-induced skeletal muscle atrophy. Full article

This review explores the dual role of skeletal muscle as both a mechanical and endocrine organ, highlighting its contributions to overall health and its adaptability to various inputs such as nutrition, hormones, exercise, and injuries. In addition to its role in metabolism and energy conversion, skeletal muscle secretes signalling molecules called myokines (at rest) and exerkines (during/after physical exercise), which communicate with other organs like the brain, the cardiovascular system, and the immune system. Key molecules such as interleukins, irisin, and myostatin are discussed for their roles in mediating muscle health and inter-organ communication. This work also focuses on the muscle–gut axis, emphasising the bidirectional interaction between skeletal muscle and the gut microbiota, a complex ecosystem influencing immune defence, digestion, and metabolism. Muscle activity, particularly exercise, alters the gut microbial composition, promoting beneficial species, while gut-derived metabolites like short-chain fatty acids (SCFAs) impact muscle metabolism, mitochondrial function, and insulin sensitivity. Dysbiosis, or an imbalanced microbiota, can lead to muscle atrophy, inflammation, and metabolic dysfunction. This evidence highlights emerging research into myokines and exerkines as potential therapeutic targets for managing conditions like muscle decline, ageing, and metabolic diseases through muscle–gut interactions. Full article

Muscular dystrophies (MDs) are genetically heterogeneous diseases characterized by primary skeletal muscle atrophy. The collapse of muscle structure and irreversible degeneration of tissues promote the occurrence of comorbidities, including cardiomyopathy and respiratory failure. Mitochondrial dysfunction leads to inflammation, fibrosis, and adipogenic cellular infiltrates that exacerbate the symptomatology of MD patients. Gastrointestinal disorders and metabolic anomalies are common in MD patients and may be determined by the interaction between the intestine and its microbiota. Therefore, the gut–muscle axis is one of the actors involved in the spread of inflammatory signals to all muscles. In this review, we aim to examine in depth how intestinal dysbiosis can modulate the metabolic state, the immune response, and mitochondrial biogenesis in the course and progression of the most investigated MDs such as Duchenne Muscular Dystrophy (DMD) and Myotonic Dystrophy (MD1), to better identify gut microbiota metabolites working as therapeutic adjuvants to improve symptoms of MD. Full article

The vagus nerve regulates metabolic homeostasis and mediates gut–brain communication. We hypothesized that vagus nerve dysfunction, induced by truncated vagotomy (VGX) or carotid artery occlusion (AO), would disrupt gut–brain communication and exacerbate metabolic dysregulation, neuroinflammation, and cognitive impairment. This study aimed to test the hypothesis in gerbils fed a high-fat diet. The gerbils were divided into four groups: AO with VGX (AO_VGX), AO without VGX (AO_NVGX), no AO with VGX (NAO_VGX), and no AO without VGX (NAO_NVGX). After 5 weeks on a high-fat diet, the neuronal cell death, neurological severity, hippocampal lipids and inflammation, energy/glucose metabolism, intestinal morphology, and fecal microbiome composition were assessed. AO and VGX increased the neuronal cell death and neurological severity scores associated with increased hippocampal lipid profiles and lipid peroxidation, as well as changes in the inflammatory cytokine expression and brain-derived neurotrophic factor (BDNF) levels. AO and VGX also increased the body weight, visceral fat mass, and insulin resistance and decreased the skeletal muscle mass. The intestinal morphology and microbiome composition were altered, with an increase in the abundance of Bifidobacterium and a decrease in Akkermansia and Ruminococcus. Microbial metagenome functions were also impacted, including glutamatergic synaptic activity, glycogen synthesis, and amino acid biosynthesis. Interestingly, the effects of VGX were not significantly additive with AO, suggesting that AO inhibited the vagus nerve activity, partly offsetting the effects of VGX. In conclusion, AO and VGX exacerbated the dysregulation of energy, glucose, and lipid metabolism, neuroinflammation, and memory deficits, potentially through the modulation of the gut–brain axis. Targeting the gut–brain axis by inhibiting vagus nerve suppression represents a potential therapeutic strategy for ischemic stroke. Full article

Sarcopenia refers to an age-related decrease in muscle mass and strength. The gut–muscle axis has been proposed as a promising target to alleviate muscle atrophy. The effect of KL-Biome—a postbiotic preparation comprising heat-killed Lactiplantibacillus plantarum KM-2, its metabolites, and an excipient (soybean powder)—on muscle atrophy was evaluated using dexamethasone (DEX)-induced atrophic C2C12 myoblasts and C57BL/6J mice. KL-Biome significantly downregulated the expression of genes (Atrogin-1 and MuRF1) associated with skeletal muscle degradation but increased the anabolic phosphorylation of FoxO3a, Akt, and mTOR in C2C12 cells. Oral administration of KL-Biome (900 mg/kg) for 8 weeks significantly improved muscle mass, muscle function, and serum lactate dehydrogenase levels in DEX-treated mice. KL-Biome administration increased gut microbiome diversity and reversed DEX-mediated gut microbiota alterations. Furthermore, it significantly increased the relative abundances of the genera Subdologranulum, Alistipes, and Faecalibacterium prausnitzii, which are substantially involved in short-chain fatty acid production. These findings suggest that KL-Biome exerts beneficial effects on muscle atrophy by regulating gut microbiota. Full article

The functions of the gut are closely related to those of many other organs in the human body. Indeed, the gut microbiota (GM) metabolize several nutrients and compounds that, once released in the bloodstream, can reach distant organs, thus influencing the metabolic and inflammatory tone of the host. The main microbiota-derived metabolites responsible for the modulation of endocrine responses are short-chain fatty acids (SCFAs), bile acids and glucagon-like peptide 1 (GLP-1). These molecules can (i) regulate the pancreatic hormones (insulin and glucagon), (ii) increase glycogen synthesis in the liver, and (iii) boost energy expenditure, especially in skeletal muscles and brown adipose tissue. In other words, they are critical in maintaining glucose and lipid homeostasis. In GM dysbiosis, the imbalance of microbiota-related products can affect the proper endocrine and metabolic functions, including those related to the gut–liver–pancreas axis (GLPA). In addition, the dysbiosis can contribute to the onset of some diseases such as non-alcoholic steatohepatitis (NASH)/non-alcoholic fatty liver disease (NAFLD), hepatocellular carcinoma (HCC), and type 2 diabetes (T2D). In this review, we explored the roles of the gut microbiota-derived metabolites and their involvement in onset and progression of these diseases. In addition, we detailed the main microbiota-modulating strategies that could improve the diseases’ development by restoring the healthy balance of the GLPA. Full article

Type 2 diabetes mellitus (T2DM) is a burgeoning public health challenge worldwide. Individuals with T2DM are at increased risk for skeletal muscle atrophy, a serious complication that significantly compromises quality of life and for which effective prevention measures are currently inadequate. Emerging evidence indicates that systemic and local inflammation stemming from the compromised intestinal barrier is one of the crucial mechanisms contributing to skeletal muscle atrophy in T2DM patients. Notably, natural plant polysaccharides were found to be capable of enhancing intestinal barrier function and mitigating secondary inflammation in some diseases. Herein, we hypothesized that Grifola frondosa polysaccharide (GFP), one of the major plant polysaccharides, could prevent skeletal muscle atrophy in T2DM via regulating intestinal barrier function and inhibiting systemic and local inflammation. Using a well-established T2DM rat model, we demonstrated that GFP was able to not only prevent hyperglycemia and insulin resistance but also repair intestinal mucosal barrier damage and subsequent inflammation, thereby alleviating the skeletal muscle atrophy in the T2DM rat model. Additionally, the binding free energy analysis and molecular docking of monosaccharides constituting GFP were further expanded for related targets to uncover more potential mechanisms. These results provide a novel preventative and therapeutic strategy for T2DM patients. Full article