Chronic diseases are often associated with increased inflammation and oxidative stress, which contribute to disease progression. Glutamine, a conditionally essential amino acid, has been studied for its potential anti-inflammatory and antioxidant properties in various chronic conditions. The present systematic review evaluates the effects of glutamine supplementation on inflammatory markers and oxidative stress indices in patients with chronic diseases. Systematic searches were performed in web databases; Web of Science, Scopus, and PubMed/Medline until May 2025, to identify related randomized controlled trials (RCTs) according to the Cochrane Library and PICOS criteria (population: individuals > 18years, intervention: glutamine, Comparison: placebo or control, Outcomes: inflammatory and oxidative stress markers in chronic diseases). The Cochrane collaboration tool was used to assess the risk of bias in clinical trials. Six RCTs that assessed the effect of glutamine supplementation on inflammation and oxidative stress markers were included in the study. In these studies, glutamine was administered to the participants through oral or parenteral routes. In three studies improve inflammation via significant reductions in CRP were observed. However, in three studies that examined TNF-α as an inflammatory marker, only one study found its levels to be significantly reduced. Also, of the two studies that examined oxidative stress levels, only one study significantly decreased the MDA and increased SOD levels, and in the other study, glutamine supplementation had no significant effect on glutathione levels. Our findings showed that glutamine supplementation might have a positive effect on inflammation and oxidative stress indices such as TNF-α, CRP, MDA, and SOD in some chronic diseases, however, these effects have not been shown in all studies, so more carefully designed clinical trial studies with different doses of glutamine on inflammation and oxidative stress in chronic diseases are needed. PROSPERO Code: This study was registered in the PROSPERO international prospective register of systematic reviews registration number: CRD420251049112.

Radiation-induced oral mucositis (RIOM) is a common and debilitating complication of radiotherapy for head and neck cancer (HNC), frequently leading to severe pain, impaired oral intake, and treatment interruption. Nutritional interventions that support mucosal integrity may reduce mucosal injury and improve recovery. To evaluate the effects of oral L-arginine and L-glutamine supplementation on the severity and recovery of radiation-induced oral mucositis and their association with salivary inflammatory and regenerative biomarkers. In this triple-blind, parallel-arm randomized clinical trial, 84 patients receiving radiotherapy for HNC were allocated to oral L-arginine, L-glutamine, or maltodextrin control three times daily from Week 2 of radiotherapy until treatment completion. RIOM severity was assessed using the WHO scale at Weeks 2, 5, and 7. Salivary interleukin-6 (IL-6), nitric oxide (NO), and epidermal growth factor (EGF) were measured. Longitudinal changes were analysed using linear mixed-effects models, and associations with mucositis severity were evaluated using correlation and receiver operating characteristic analyses. At Week 5, severe mucositis occurred in 92.9% of controls compared with 17.9% and 3.6% in the arginine and glutamine groups (p < 0.001). Intervention groups showed lower IL-6 and NO levels and higher EGF levels (p < 0.001). Biomarkers were significantly correlated with mucositis severity, and IL-6 demonstrated excellent discrimination of severe mucositis (AUC = 0.988). Oral arginine and glutamine supplementation was associated with reduced severity and enhanced recovery of RIOM. Nutritional amino acid supplementation may represent a useful adjunct in supportive oral care and oral rehabilitation for patients undergoing radiotherapy. The study was prospectively registered at ClinicalTrials.gov (Identifier: NCT07020754) on June 6, 2025.

Severe traumatic injury triggers a profound hypermetabolic and hypercatabolic response, marked by increased resting energy expenditure, accelerated protein breakdown, muscle wasting, and heightened risk of malnutrition, infection, and mortality. Timely and targeted nutritional intervention is therefore essential to support immune function, promote wound healing, and facilitate recovery. Herein, we examine the metabolic demands of patients with severe trauma and synthesize current clinical guidelines and evidence-based strategies for nutritional management. This review outlines the neuroendocrine, inflammatory, and metabolic mechanisms that drive hypercatabolism following major trauma. It evaluates methods for estimating energy expenditure and their limitations, and discusses recommended caloric and protein targets, as well as timing of initiation and preferred routes of nutritional support. Additionally, our review examines the evidence for adjunctive immunonutrition, including supplementation of glutamine, omega-3 fatty acids, arginine, and ghrelin. In summary, early and individualized nutritional therapy is critical to mitigating hypercatabolism and improving clinical outcomes in trauma patients. Although foundational guidelines have been established, high-quality randomized controlled trials remain necessary to better define the role of specific immunonutrients across diverse trauma populations.

Pancreatic adenocarcinoma (PAAD) is characterized by profound metabolic reprogramming, including altered branched-chain amino acid (BCAA) metabolism. While the tumor-promoting role of branched-chain aminotransferase 2 (BCAT2) in PAAD has been well documented, the function of branched-chain aminotransferase 1 (BCAT1) remains unclear, particularly in PAAD cells with low endogenous BCAT1 expression. This study aimed to define the context-dependent role of BCAT1 in PAAD and to elucidate the underlying molecular mechanisms. The expression of BCAT1 and BCAA metabolism-related molecules was assessed by Western blotting and quantitative reverse transcription polymerase chain reaction (qRT-PCR). The effects of BCAT1 and SLC3A2 on PAAD cell proliferation were evaluated using CCK-8 assays in vitro and xenograft nude mouse models in vivo. Astral DIA proteomics and LC-MS-based untargeted metabolomics were performed to characterize protein and metabolic alterations induced by BCAT1 overexpression or SLC3A2 depletion. Stable SLC3A2-knockdown PAAD cell lines were established by lentiviral transduction. Seahorse XFe96 analysis was used to assess cellular bioenergetics by measuring the oxygen consumption rate (OCR) and extracellular acidification rate (ECAR). BCAT1 expression was markedly reduced in multiple PAAD cell lines, and ectopic BCAT1 overexpression significantly inhibited PAAD cell proliferation both in vitro and in vivo. Mechanistically, BCAT1 overexpression suppressed Akt/mTOR signaling, impaired mitochondrial respiration and glycolytic activity, and disrupted glutamine metabolism, glutathione metabolism, and nucleotide biosynthesis. Notably, intracellular BCAA levels were not significantly altered, whereas glutamine was markedly reduced. Glutamine supplementation partially rescued the BCAT1-induced inhibition of Akt/mTOR signaling and cell growth. Proteomic analysis further revealed that BCAT1 overexpression reduced SLC3A2 expression, and SLC3A2 depletion phenocopied the effects of BCAT1 overexpression on glutamine metabolism, bioenergetics, Akt signaling, and tumor growth. Mechanistically, BCAT1 promoted SLC3A2 degradation through a BTRC-dependent proteasomal pathway, thereby restricting glutamine uptake and reducing intracellular nucleotide availability. BCAT1 functions as a context-dependent tumor suppressor in PAAD. In BCAT1-low PAAD cells, BCAT1 overexpression inhibits tumor growth by promoting BTRC-dependent proteasomal degradation of SLC3A2, thereby limiting glutamine uptake and suppressing Akt/mTOR signaling, cellular bioenergetics, and nucleotide biosynthesis, despite minimal changes in intracellular BCAA levels. These findings identify the BCAT1-BTRC-SLC3A2 axis as a previously unrecognized metabolic regulatory pathway in PAAD and suggest a potential therapeutic strategy for targeting tumor metabolic vulnerabilities.

BackgroundParenteral glutamine (Gln) supplementation can enhance the immune function of patients with colorectal cancer(CRC), regulate inflammatory response, nitrogen balance and protein synthesis, reduce the morbidity of postoperative complications and shorten the length of hospitalization. However, some guidelines and clinical studies have questioned the rationality of using glutamine-containing immunonutrition support in the perioperative period of CRC. Therefore, we conducted a meta-analysis of the effects of perioperative glutamine-enriched parenteral nutrition on short-term postoperative clinical outcomes in patients with CRC.MethodsA comprehensive search of all relevant literature from the default date to June 2025 was performed using the following databases: PubMed, Embase, Web of Science, Cochrane Library, China Biology Medicine Database (CBM), China National Knowledge Infrastructure (CNKI), VIP Medical Information System (VIP), and Wanfang electronic database. RevMan 5.3 software was used for the meta-analysis. We calculated the outcomes using random- and fixed-effects models.ResultsSeventeen single-center randomized controlled trials (RCTs) involving 950 patients with CRC were included. The control group consisted of 470 patients who received traditional parenteral nutrition therapy and the experimental group consisted of 480 patients who received parenteral nutrition with Gln. The analyses showed that perioperative Gln-enhanced parenteral nutrition reduced the morbidity of infectious complications (Relative Risk [RR]=0.36,95% Confidence Interval [CI]:0.23-0.58) and non-infectious complications (RR=0.27, 95% CI: 0.13-0.55). The length of hospitalization was reduced by 2.18 days (mean difference [MD] = -2.18, 95% CI: -2.59--1.78).ConclusionParenteral Gln supplementation may potentially reduced the morbidity of postoperative complications, shortened postoperative hospitalization, improved some aspects of nutritional status, immune and inflammation function in patients with CRC, based on current evidence of low-to-moderate certainty.

Intense physical activity imposes substantial oxidative, metabolic, and immunological stress on the human body. It is often accompanied by reductions in plasma glutamine levels, making this amino acid conditionally essential. Glutamine plays a vital role in energy production, nitrogen transport, acid-base balance, antioxidant defense, and immune function. It is required in the biosynthesis of neurotransmitters, nucleotides, nicotinamide-derived coenzymes, glutathione, and hexosamines, making it a candidate for supporting exercise recovery. In addition, glutamine may support key mechanisms involved in muscle adaptation and recovery during exercise-induced stress by contributing to redox balance, energy sensing, anabolic signaling, intestinal barrier integrity, and immune function. This narrative review aims to synthesize biochemical mechanisms underlying glutamine effects relevant to exercise and evaluate preclinical and clinical findings on supplementation outcomes, with emphasis on timing strategies. Preclinical findings demonstrate that glutamine can modulate protein synthesis, reduce oxidative stress, improve intestinal integrity, and attenuate immune and inflammatory disturbances. Limited preclinical data suggest that post-exercise supplementation may better resolve muscle and organ damage. Clinical trials, however, report heterogeneous outcomes: several studies show improvements in markers of intestinal permeability and intestinal epithelial damage, oxidative stress, muscle damage, and inflammation, whereas others report minimal or no effect, including limited influence on performance outcomes. Variability in timing protocols, participant characteristics, and measured endpoints contributes to inconsistent findings. Overall, glutamine demonstrates several biologically plausible mechanisms that could support recovery and overall health in active individuals, athletes, and specific clinical populations. However, current evidence remains insufficient to determine clear supplementation benefits or define an optimal timing strategy. Future research using standardized protocols and integrated biochemical and functional endpoints is needed to clarify timing effects. Until such evidence emerges, recommendations should remain individualized, considering athlete-specific needs.

Hypothalamic inflammation plays a key pathophysiological mechanism linking chronic consumption of a high fat diet (HFD) to the development of obesity and associated metabolic complications. Pilot studies report that oral glutamine (Gln) supplementation might reduce waist circumference and improve metabolic and inflammatory status in obesity patients. Although Gln metabolism plays a key role in intercellular communication in the central nervous system, its potential beneficial effects remain unexplored in these contexts. Here, we aimed to evaluate how stress and glutamine supplementation can modulate the hypothalamic response to HFD in mice using a chronic-restraint stress (CRS) model, which mimics IBS symptoms. From week 12 to week 14, mice received or not Gln diluted in drinking water (2g/kg/day) and were placed in restraint tubes (2h/day) for the last four consecutive days of protocol. Male and female obese mice showed a difference in vulnerability to CRS-induced effects. Moreover, mice responded to Gln supplementation in a sex-dependent manner, especially in stress conditions. Hypothalamic pathways regulating energy homeostasis were more impacted in male mice, whereas factors involved in neuroinflammation were more affected in female mice. Gln supplementation led to an increase in Mc4r and Bdnf mRNA levels and GFAP expression in male mice, while upregulated Iba1 and Il6 mRNA levels as well as signs of microgliosis were observed in stressed females. In conclusion, mice with obesity showed sex-specific hypothalamic response to glutamine supplementation and stress. Further investigations should be done to decipher underlying mechanisms.

Introduction: hematopoietic stem cell transplantation (HSCT) is an aggressive and toxic procedure that can lead to malnutrition in patients. It has been proposed that these conditions may worsen under conditions of glutamine deficiency. Aim: the aim of this study is to analyze the effect of glutamine supplementation in parenteral nutrition (PN) for patients undergoing HSCT. Material and methods: a retrospective observational study was conducted on patients who received PN following HSCT (both autologous and allo-HSCT) at our hospital between 2015 and 2020. The patients were divided into two groups: those who received glutamine and those who did not. Nutritional status, duration of PN, associated complications, hospital stay, mortality, and progression-free survival (PFS) at day +100 were analyzed. Data analysis was performed using the SPSS statistical software package. Results: a total of 117 patients were included, 41.9 % of whom received glutamine supplementation in their PN. There were no significant differences in nutritional status or duration of PN between the two groups. Infections were more frequent in the glutamine group (p = 0.05). There were no significant differences between groups for other complications, although a subgroup analysis based on the type of conditioning showed a higher prevalence of diarrhea in the non-glutamine group of patients receiving reduced-intensity conditioning (p = 0.02). There were no significant differences in mortality, PFS, or duration of PN. Hospital stays were longer in the glutamine group (p = 0.026). Conclusions: in our study, patients receiving glutamine did not show an improvement in their nutritional status; they experienced more infections and had longer hospital stays. We suggest that glutamine supplementation should not be routinely recommended for PN in these patients.

Oral glutamine supplementation in dogs infected with canine parvovirus type 2.

Shen Ling Bai Zhu San promotes gut IgA+ plasma cells to alleviate chronic diarrhea in mice via increasing systematic glutamine.

IntroductionAllergic rhinitis (AR) is classically regarded as a type 2 immune-driven disease, yet its chronicity and heterogeneity suggest that additional regulatory layers shape the local immune microenvironment. Although immune cell function is closely linked to metabolic state, how specific metabolic cues are integrated into immune signaling in AR remains unclear.MethodsWe combined human nasal mucosal metabolomic analysis, murine models, single-cell transcriptomics, bulk RNA sequencing, and protein assays to investigate the role of glutamine in AR pathophysiology.ResultsWe identified elevated glutamine levels in AR nasal mucosa and found that dietary glutamine supplementation was associated with altered nasal behavioral responses in experimental AR. Single-cell profiling revealed changes in immune cell composition, with macrophages displaying a shift toward an M2-like transcriptional state under high-glutamine conditions. Transcriptomic and pathway analyses positioned fibroblast growth factor receptor 1 (FGFR1) within differentially enriched signaling networks, and its expression increased under high-glutamine conditions. Protein-level assays further showed that aminoacylation-associated signals on FGFR1 varied with glutamine availability, together with coordinated changes in YARS and SIRT1.DiscussionThese hypothesis-generating findings support an associative model in which metabolic alterations in AR are linked to non-canonical modification of FGFR1 and macrophage transcriptional polarization, suggesting a potential immunometabolic layer regulating the nasal mucosal microenvironment.

BackgroundGlutamine, an essential nutrient for healthy cells, supports immunity and cytoprotection during anticancer treatments. However, intense glutaminolysis may promote proliferation and chemoresistance in ovarian carcinomas by activating the PI3K/AKT/mTORC1 pathway and overexpressing c-Myc. This study aimed to characterize glutamine metabolism in ovarian carcinomas and assess its impact on tumor aggressiveness and chemosensitivity, to inform nutritional supplementation or therapeutic targeting.MethodsGlutamine and glucose consumption, chemosensitivity to cisplatin and paclitaxel, and doubling time were analyzed in three ovarian carcinoma cell lines (ES-2, TOV-21G: clear cell; OVCAR-3: serous papillary) and primary ascites cells under varying glutamine concentrations (0.5, 1, 2, 4 mM). Expression of glutaminase, glutamate dehydrogenase 1 (GDH1), and c-Myc, as well as PI3K/AKT/mTORC1 activation, were assessed by reverse transcription-polymerase chain reaction (RT-PCR) and Western blot.ResultsTOV-21G exhibited significantly higher glutamine consumption (13.3±1.3 vs. 6.5±0.3 and 7±0.5 U/mg protein, P<0.001), increased expression of glutaminase, GDH1, and c-Myc, marked PI3K/AKT/mTORC1 activation (P=0.045), and a shorter doubling time (11.5±1.5 h, P=0.04) compared to ES-2 and OVCAR-3. OVCAR-3 showed significantly greater resistance to cisplatin and paclitaxel (P=0.03). Varying glutamine concentrations did not affect chemosensitivity.ConclusionsIntense glutaminolysis is associated with increased tumor aggressiveness, suggesting a prognostic role for 18F-(2S,4R)-4-fluoroglutamine (18F-fluoroglutamine) positron emission tomography (PET) imaging. Glutamine supplementation, without impacting chemoresistance, may mitigate iatrogenic effects, while targeting glutaminolysis offers a therapeutic perspective.

Biallelic mutations in SLC38A3 lead to postnatal progressive microcephaly, epilepsy, and intellectual disability. However, the underlying pathophysiology remains unknown. Here, we identified Slc38a3 expressed at the vascular endothelium as a critical glutamine transporter that mediates blood-to-brain influx of glutamine through the blood-brain barrier (BBB). Endothelial selective deletion of Slc38a3 (Slc38a3-cKO) lowered the influx of glutamine across the BBB and decreased brain glutamine levels in mouse pups. This was associated with lower transfer of glutamine carbons to glutamate and GABA, suggesting impairment of the glutamine-glutamate/GABA metabolic cycle. Like individuals with mutations in SLC38A3, Slc38a3-cKO pups developed postnatal progressive microcephaly as well as behavioural impairments and morphological alterations in synapses. Approximately 30% of Slc38a3-cKO pups fail to thrive, exhibiting motor dysfunction and preweaning lethality. Glutamine deficiency in the Slc38a3-cKO hippocampus was associated with a slower TCA cycle and a seemingly adaptive increase in glycolysis rate. Glutamine supplementation replenished brain glutamine, prevented microcephaly, and normalized motor behavior in Slc38a3-cKO pups, indicating that brain glutamine deficiency is the primary cause of the phenotype. In contrast to the dogma that all glutamine is produced locally in the brain, our data show that Slc38a3 provides blood-derived glutamine for neurotransmitter synthesis, energy metabolism, and synaptogenesis. Our findings suggest that SLC38A3 mutations cause a glutamine-related BBB aminoacidopathy and developmental disorder, which may be amenable to glutamine supplementation therapy.

The gestational period is a critical developmental window where maternal nutrition programs offspring growth and long-term health. This study evaluated dietary rumen-protected glutamine (RP-Gln) supplementation during late gestation on lamb growth performance, and its regulatory effects on metabolic, immune, and microbial parameters in ewes and offspring. Compared with controls, moderate RP-Gln significantly improved lamb growth, increasing birth weight, 15-day body weight, and average daily gain (p < 0.01). In ewes, RP-Gln elevated serum GGT activity (p < 0.05), improved lipid metabolism, and reduced offspring muscular stress. Antioxidant capacity was enhanced in both ewes and lambs, with higher antioxidant enzyme activities and lower MDA levels (p < 0.05). RP-Gln also remodeled gut microbiota by promoting beneficial genera like Lactobacillus and Faecalibacterium, and reinforcing dam-offspring microbial transmission. Metabolomics revealed elevated polyunsaturated fatty acids, vitamin C, and tyrosine derivatives in ewes, and enhanced aromatic amino acid biosynthesis in lambs. In summary, glutamine supplementation in late-gestation ewes enhances maternal antioxidant and anti-inflammatory capacity, optimizes gut microbiota, and stimulates n-3 PUFA synthesis. These benefits are transmitted to the fetus, improving offspring antioxidant function, immune regulation, and intestinal health. Glutamine also promotes aromatic amino acid synthesis while inhibiting the tryptophan-kynurenine pathway, collectively supporting lamb growth and health.

AGC1 deficiency is a rare, early-onset encephalopathy caused by mutations in the SLC25A12 gene, encoding the mitochondrial aspartate/glutamate carrier isoform 1 (AGC1). Patients exhibit epileptic encephalopathy, cerebral hypomyelination, severe hypotonia, and global developmental delay. A hallmark biochemical feature of AGC1 deficiency is reduced brain N-acetylaspartate (NAA), a key metabolite involved in myelin lipid synthesis. However, the underlying mechanisms leading to the hypomyelinating phenotype remain unclear. In this study, we generated neuronal progenitors (NPs) derived from human-induced pluripotent stem cells (hiPSCs) of AGC1-deficient patients to investigate the metabolic and bioenergetic consequences of AGC1 loss. We demonstrated that AGC1-deficient NPs exhibit impaired proliferation, increased apoptosis, and a metabolic shift toward a hyperglycolytic phenotype due to defective mitochondrial pyruvate oxidation. RNA sequencing revealed downregulation of mitochondrial pyruvate carrier MPC1/2, limiting pyruvate-driven oxidative phosphorylation (OXPHOS) and reinforcing glycolysis as the primary energy source. Despite this metabolic shift, AGC1-deficient mitochondria retained the potential for OXPHOS when alternative anaplerotic substrates were provided. Notably, the administration of ketone bodies, in combination with glutamine, fully restored mitochondrial respiration, suggesting a mechanistic basis for the clinical improvements observed in AGC1-deficient patients undergoing ketogenic diet therapy. Our study highlights the importance of alternative metabolic pathways in maintaining neuronal energy homeostasis in AGC1 deficiency and offers insights into potential therapeutic strategies aimed at bypassing the mitochondrial pyruvate oxidation defect.

ABSTRACT In the Qinghai–Tibet Plateau, the low temperatures and the brief forage‐growing season result in starvation in yaks and cause growth retardation. We aim to study the effects of Glutamine (Gln) on rumen epithelium damage induced by feed restriction (FR) in yaks. Eighteen healthy female yaks (264.3 ± 27.83 kg) were randomly divided into three groups (6 yaks in each group). The growth experiment lasted for 60 days after 15 days of pre‐feeding. Control (Con) group was fed normal feed, feed restriction (FR) group was fed 50% feed intake of the pre‐feeding period, feed restriction + glutamine (FR + Gln) group was fed 50% feed intake during day 0–30, and was fed 50% feed intake + 1% Gln during day 31–60. The results showed that FR significantly decreased 11.66% of rumen weight and 44.26% of the rumen epithelial papillae height ( p &lt; 0.05). However, compared with the FR group, the rumen epithelial papillae height increased significantly by 42.16% ( p &lt; 0.05). Besides, FR decreased the Gln metabolism, adenosine triphosphate (ATP) levels, and mitochondrial DNA (mtDNA) copy number, increased the reactive oxygen species levels, inhibited the proliferation of rumen epithelial cells, and induced apoptosis ( p &lt; 0.05), whereas Gln alleviated them ( p &lt; 0.05). This study provided theoretical guidance for the protection of female yak farming in the Qinghai–Tibet Plateau during the cold season.

Background: Ventilator-associated pneumonia (VAP) is a common and serious complication of mechanical ventilation in intensive care units (ICUs). The current study evaluates the effectiveness of enteral glutamine (GLN) supplementation in preventing VAP in ICU patients. Methods: This controlled, randomized clinical trial was performed on mechanically ventilated ICU patients who had a Clinical Pulmonary Infection Score (CPIS) of ≤ 6 within 48 hours of starting ventilation. Patients in the intervention group received 40 g of GLN during the first 48 hours after intubation, and this was continued for seven days. Both the intervention and control groups received standard preventive care. Outcomes were evaluated by comparing the incidence of VAP, the number of pneumonia-free days, and the duration of ventilation and ICU length of stay in each group. Results: We analyzed the medical records of 613 patients to identify those who met the eligibility criteria for our study, resulting in a final cohort of 35 participants (16 in the intervention group and 19 in the control group). The present clinical trial did not reach its target sample size of 23 patients per group, primarily because of participant attrition and loss to follow-up. Our findings revealed no significant differences in the incidence of early, late, or overall VAP between the two groups. However, the number of pneumonia-free days was significantly higher in the intervention group compared to the control group (log-rank test: P-value= 0.05). Other secondary outcomes, such as mortality rate, and the duration of ICU stay, hospital stay, and mechanical ventilation, also showed no significant differences between the two groups. Conclusion: The administration of oral GLN supplements has been associated with an increase in the number of pneumonia-free days among ICU patients; however, this benefit does not appear to reduce the incidence of VAP. Further high-quality studies are warranted to validate these observations and to investigate the potential efficacy of GLN supplementation within specific patient cohorts.

Preoperative physical frailty is a significant predictor of adverse postoperative outcomes in older patients undergoing cardiac surgery. Inflammation plays a crucial role in the development of frailty and contributes to postoperative complications. This study investigated the effects of preoperative beta-hydroxy-beta-methylbutyrate (HMB), arginine, and glutamine supplementation on inflammatory markers, nutritional status, and renal function in older patients undergoing cardiac surgery. This was a secondary analysis of a single-center, open-label, randomized controlled trial. Patients aged ≥65 years scheduled for elective cardiac surgery were randomized to receive either HMB supplementation (1200 mg HMB, 7000 mg l-glutamine, and 7000 mg L-arginine, twice daily) or routine care for at least two weeks before surgery. Serum levels of tumor necrosis factor-alpha (TNF-α), and other biochemical markers were measured at baseline, pre-surgery, and two weeks post-surgery. Forty-four patients (mean age 72.5 years, 36 % women) were analyzed. Preoperative HMB supplementation significantly reduced pre-surgery serum TNF-α levels compared to the control group (0.85 ± 0.28 pg/mL vs. 1.10 ± 0.44 pg/mL, p = 0.039). However, this difference was not observed two weeks post-surgery. No significant differences were observed in C-reactive protein levels or other nutritional markers between the two groups at any time point. Preoperative supplementation with a combination of HMB, glutamine, and arginine was effective in reducing preoperative TNF-α levels in older patients undergoing cardiac surgery, suggesting a potential anti-inflammatory effect. This anti-inflammatory effect suggests a potential mechanism for improving postoperative outcomes and warrants further investigation. Registration number of Clinical Trial: UMIN000030490 (https://upload.umin.ac.jp/cgi-open-bin/ctr_e/ctr_view.cgi?recptno=R000034773).

Effects of a diet containing glutamine on the slaughter performance, meat quality, and skeletal muscle fiber types of feed-restricted yaks.

Effects of dietary glutamine supplementation on lipid metabolism, fatty acid composition, and taste properties in the longissimus thoracis muscle of feed-restricted yaks