Search Results (322)

Background/Objectives: Circulating amino acid concentrations and their excretion can provide insights into dietary protein intake and metabolism. Alterations in amino acid homeostasis occur in various disorders due to nutritional imbalances or metabolic changes, including obesity. A ketogenic diet (KD) has gained popularity for weight management; however, its metabolic effects are not fully known. Therefore, the aim of this study was to evaluate the effect of an eight-week, energy-restricted Mediterranean-type KD on the amino acid metabolism in women with overweight and class I obesity. Methods: A randomized, single-center, controlled trial was conducted with 80 women with a BMI of 25.5–35 in age between 18 and 45 years, without any chronic diseases. Randomly divided women received food catering with approximately 1750 kcal daily for eight weeks, containing KD or standard diet (STD), respectively. The concentration of amino acids was assessed by gas chromatography-mass spectrometry after the derivatization with chloroformate in serum and urine collected at the baseline, after 4 weeks, and at the end of the intervention. Results: The results collected from 66 participants were included in the final analyses. Independent of diet type, weight reduction was associated with increased circulating α-aminobutyric acid and decreased proline, glutamate, and tyrosine. The KD led to lower concentrations of alanine, methionine, threonine, and tryptophan, alongside higher levels of branched-chain amino acids (BCAA) and α-aminobutyric acid compared to the STD. Urinary amino acid excretion decreased after weight reduction. KD was associated with higher urinary excretion of BCAA and β-aminoisobutyric acid. Conclusions: In summary, both weight reduction and KD significantly affect the amino acid metabolism, which might have implications for inflammation, oxidative stress, and cardiometabolic risk. Full article

Drought stress severely impacts agricultural productivity, yet mechanisms underlying microbial enhancement of plant drought tolerance remain poorly understood. This study investigated whether Sphingobacterium nripensae DR205 exhibits drought-specific plant growth promotion through conditional metabolic activation. We combined plant cultivation experiments, genome sequencing, and comparative transcriptomics to evaluate DR205 responses under normal and drought conditions with or without root exudates. DR205 showed minimal growth promotion under normal conditions but enhanced plant biomass by 74–344% specifically under drought stress. Genome analysis revealed complete pathways for both stress tolerance (osmolyte biosynthesis and antioxidant systems) and plant interaction (IAA production and nutrient mobilization). Transcriptomics uncovered dramatic metabolic reprogramming under drought, with branched-chain amino acid (BCAA) biosynthesis genes shifting from 27-fold suppression under root exudates to 17-fold upregulation under drought. Lysine biosynthesis showed similar drought-specific activation patterns. Critically, drought signals overrode plant signals maintaining BCAA activation regardless of root exudate presence and ensuring metabolic investment in plant support occurred specifically during water deficit. This conditional mutualism represents a novel bacterial strategy where plant support is selectively activated during environmental stress. These findings challenge conventional PGPR paradigms and offer new approaches for developing climate-resilient agricultural systems through targeted application of stress-responsive beneficial microbes. Full article

Background: Branched-chain amino acids (BCAAs) are popular as sports supplements due to their ability to enhance performance and recovery. However, the full spectrum of metabolic alterations triggered by acute supplementation with BCAAs in conjunction with exercise remains incompletely understood. Methods: A randomized crossover trial was conducted in 8 healthy active young males, who received either BCAA or placebo supplementation for three consecutive days prior to a high-intensity cycling test. Plasma samples were collected pre- and post-exercise and analyzed by ultra-high-performance liquid chromatography–quadrupole time-of-flight mass spectrometry, followed by correlation and enrichment analyses. Results: Acute BCAA supplementation was significantly associated with enhanced fat oxidation and attenuated post-exercise increases in plasma ammonia, creatine kinase, and lactate dehydrogenase, suggesting the potential improvements in energy supply and membrane stability. Metabolomics analysis identified differential metabolites primarily involved in lipid, amino acid, and glucose metabolism. Pathway enrichment revealed coordinated regulation of fatty acid oxidation (FAO) and tryptophan-related pathways. Correlation analysis further showed that changes in metabolite profiles were strongly associated with biochemical outcomes, particularly linking enhanced fat oxidation and ammonia clearance with BCAA intake. Conclusions: Short-term BCAA supplementation could enhance FAO and membrane stability via coordinated regulation of lipid and amino acid metabolism post exercise, supporting its potential role as a precision nutrition strategy. Full article

Copper and nickel ions play pivotal, albeit distinct, roles as essential trace elements in living systems, and primarily serve as co-factors for a range of enzymes. However, as with all trace metal ions, excessive concentrations can exert adverse toxicological properties. Interestingly, the incorporation of these in cell culture media can establish novel chemical interactions, with their speciation status markedly influencing characteristics, including cell maturation, and cellular uptake mechanisms. Thus, the primary objective of this study was to investigate and determine the speciation status (i.e., complexation) of nickel(II) and copper(II) ions by biomolecules present in RPMI 1640 mammalian cell culture medium using virtually non-invasive high-resolution proton NMR analysis, an investigation of much relevance to now routine studies of their toxicological actions towards cultured cells. Samples of the above aqueous culture medium were ¹H NMR-titrated with increasing added concentrations of 71–670 µmol/L Ni(II)(aq.), and 0.71–6.7, 7.1–67 and 71–670 µmol/L Cu(II)(aq.), in duplicate or triplicate. ¹H NMR spectra were acquired on a JEOL ECZ-600 spectrometer at 298 K. Results demonstrated that addition of increasing concentrations of Ni(II) and Cu(II) ions to the culture medium led to the selective broadening of a series of biomolecule resonances, results demonstrating their complexation by these agents. The most important complexants for Ni(II) were histidine > glutamine > acetate ≈ methionine ≈ lysine ≈ threonine ≈ branched-chain amino acids (BCAAs) > asparagine ≈ aspartate > tyrosine ≈ tryptophan, whereas for Cu(II) they were found to be histidine > glutamine > phenylalanine ≈ tyrosine ≈ nearly all remaining aliphatic metabolites (particularly the wealth of amino acids detectable) > 4-hydroxyphenylacetate (trace culture medium contaminant), in these orders. However, Cu(II) had the ability to influence the linewidths of these signals at much lower added levels (≤7 µmol/L) than that of Ni(II), the broadening effects of the latter occurring at concentrations which were approximately 10-fold greater. Virtually all of these added metal ion-induced resonance modifications were, as expected, reversible on addition of equivalent or excess levels of the chelator EDTA. From this study, changes in the co-ordination sphere of metal ions in physiological environments can give rise to marked modifications in their physicochemical properties (e.g., redox potentials, electronic charges, the potential catalytic generation of reactive oxygen species (ROS), and cell membrane passages). Moreover, given that the above metabolites may also function as potent hydroxyl radical (^●OH) scavengers, these findings suggest that generation of this aggressively reactive oxidant directly from Cu(II) and Ni(II) ions in physiologically-relevant complexes may be scavenged in a ‘site-dependent’ manner. This study is of further relevance to trace metal ion research in general since it enhances our understanding of the nature of their interactions with culture medium biomolecules, and therefore provides valuable information regarding their overall chemical and biological activities, and toxicities. Full article

Sestrin2 (SESN2) is a highly conserved stress-inducible protein that serves as a central hub for integrating cellular responses to nutrient availability, oxidative stress, and endoplasmic reticulum (ER) stress. A key function of SESN2 is its role as a direct sensor for the branched-chain amino acid (BCAA) leucine, which modulates the activity of the mechanistic target of rapamycin complex 1 (mTORC1), a master regulator of cell growth and metabolism. While the functional link between leucine and SESN2 is well-established, the precise molecular determinants that confer its high specificity for leucine over other BCAAs, such as isoleucine and valine, remain poorly understood. This study employs an integrated computational approach, spanning atomic interactions to global protein dynamics, combining molecular docking, extensive all-atom molecular dynamics (MD) simulations, and binding free energy calculations, to elucidate the structural and dynamic basis of BCAA-SESN2 recognition. Our thermodynamic analysis reveals a distinct binding affinity hierarchy (Leucine > Isoleucine > Valine), which is primarily driven by superior van der Waals interactions and the shape complementarity of leucine’s isobutyl side chain within the protein’s hydrophobic pocket. Critically, a quantitative analysis of the conformational ensemble reveals that leucine induces a dramatic collapse of the protein’s structural heterogeneity. This “conformational locking” mechanism funnels the flexible, high-entropy unbound protein—which samples 35 distinct conformations—into a sharply restricted ensemble of just 9 stable states. This four-fold reduction in conformational freedom is accompanied by a kinetic trapping effect, which significantly lowers the rate of transitions between states. This process of conformational selection stabilizes a well-defined, signaling-competent structure, providing a comprehensive, atom-to-global-scale model of SESN2’s function. In the context of these findings, this work provides a critical framework for understanding SESN2’s complex role in disease and offers a clear rationale for the design of next-generation allosteric therapeutics. Full article

Branched-chain amino acids (BCAAs) are essential amino acids in humans, with reported anti-proliferative effects on HepG2 hepatoma cells and the potential to reduce hepatocellular carcinoma (HCC) development in cirrhotic patients. PDCD4, a tumor suppressor that is downregulated in many cancers, is also suppressed by serum, EGF, or TPA treatment. This study examined the effect BCAA has on PDCD4 expression and related cellular pathways in Huh7 hepatoma cells. Cells were treated with different concentrations of BCAA, and analyzed by Western blotting, qRT-PCR, and immunofluorescence staining. Treatment with BCAA upregulated the protein levels of PDCD4, while downregulating its mRNA levels. BCAA enhanced the phosphorylation of mTORC1 substrate 4E-BP1, p70S6K1, and p70S6K1 substrate S6 ribosomal protein. BCAA also elevated the protein levels of autophagy factors p62 and ATG5 while reducing LC3-II particle formation, thus indicating impaired autophagy. ULK1 knockdown also upregulated the protein levels of PDCD4 and p62. Additionally, BCAA upregulated the phosphorylation of ULK1 at serine 757, which was inhibited by rapamycin. These findings suggest that BCAA inhibits autophagy through the mTORC1-mediated phosphorylation of ULK1 at serine 757, thereby impairing autophagosome formation and upregulating the PDCD4 protein levels by inhibiting its degradation via autophagy. Furthermore, FACS analysis showed that BCAA inhibited the proliferation of Huh7 cells. BCAA may have a preventive effect against tumor development through the modulation of autophagy and the tumor suppressor pathways. Full article

Background/Objectives: Hip fracture patients commonly exhibit impaired nutritional status, including low serum albumin levels related to sarcopenia, which may affect recovery. This study evaluated the effect of branched-chain amino acid (BCAA) supplementation on serum albumin levels in hip fracture patients. Methods: This retrospective analysis was conducted at a single tertiary referral center on a cohort of patients with hip fractures including femoral neck and intertrochanteric fractures who visited the emergency department between January 2022 and November 2023. After propensity score matching, 106 patients were analyzed (BCAA: n = 53; control: n = 53); prior to matching, 67 treated and 110 control patients were eligible. Patients receiving BCAA supplementation were administered three times daily for six weeks postoperatively and they were matched with controls based on clinical and demographic variables. Controls received standard perioperative care without BCAA supplementation, and no placebo was administered. Serum albumin levels were measured before the surgery and 6 weeks postoperatively. After propensity score matching, 53 patients from each cohort were analyzed. The primary outcome was the difference in serum albumin levels; secondary outcomes were the length of hospital stay (LOS), blood transfusions (Tf), and the incidence of delirium. Results: The matched cohorts exhibited comparable baseline characteristics. Analysis revealed a significant increase in serum albumin levels among patients who received BCAA supplementation compared to the matched control group. No differences were found in terms of LOS, Tf, and the incidence of delirium during the index admission. Conclusions: This preliminary study suggests a potential positive effect of BCAA supplementation on serum albumin levels in patients with hip fractures. Further prospective investigations with larger sample sizes are warranted to validate these findings and elucidate the clinical implications for nutritional support in this population. Full article

Ovarian cancer stem cells (OCSCs) possess stemness; differentiation capacity; and tolerance to oxidative, metabolic, and therapeutic stress, driving recurrence and chemoresistance. Emerging evidence highlights a synergistic interplay between redox homeostasis and amino acid metabolism in maintaining stemness and treatment resistance. This review integrates redox regulation, amino acid metabolic reprogramming, and tumor microenvironment (TME) signals into a unified “redox–amino acid–TME” framework. OCSCs balance signal transduction and antioxidant defense by fine-tuning reactive oxygen species (ROS) levels. Glutamine, serine/glycine, and sulfur amino acid metabolism collectively generate NADPH and glutathione, sustaining the GPX4/TRX antioxidant systems and suppressing ferroptosis. Branched-chain amino acid (BCAA)–mTOR and tryptophan (Trp)–aryl hydrocarbon receptor (AhR) axes couple amino acid sensing to redox signaling, stabilizing the stem-like phenotype. Under TME stress, including hypoxia, acidity, and nutrient competition, exosomes and stromal components reinforce stemness and immune evasion through metabolic and redox crosstalk. Therapeutically, targeting glutamine metabolism (ASCT2/GLS), serine biosynthesis (PHGDH/SHMT), or antioxidant defenses (xCT/GPX4) disrupts reducing power, increases oxidative stress, and enhances the efficacy of chemotherapy, PARP inhibition, and immunotherapy. Biomarkers such as xCT/GPX4 expression, PHGDH levels, Nrf2 activity, and GSH/NADPH ratios may guide patient stratification and response prediction. Overall, understanding the redox–amino acid metabolic network provides a mechanistic basis and translational opportunities for precision metabolic therapies in ovarian cancer. Full article

Deep venous thrombosis (DVT) is characterized by the formation of a thrombus within deep veins. The unmet need to identify new biomarkers and causal risk factors in DVT patients has led to the use of novel techniques, such as metabolite analyses. This study aimed to characterize metabolic alterations in acute DVT patients using ¹H-NMR spectroscopy and determine the persistence of these changes over a six-month follow-up. Metabolomics, particularly ¹H-NMR spectroscopy, was performed on serum samples from acute DVT patients (first 30 days from diagnosis) and healthy controls (HC). Additionally, 10 plasma markers were evaluated using a Luminex kit. A total of 30 patients, with a mean age of 44 ± 12.5 years, primarily women (9 males:21 females), were included. Acute DVT patients showed elevated inflammatory markers, such as IL-6, IL-8, PDGF-AB/BB, and P-selectin, which later decreased in the follow-up group. However, adhesion molecules like sVCAM-1 and sICAM-1 have increased after six months. Metabolomics analysis revealed significantly decreased levels of glutamine, glucose, and branched-chain amino acids (BCAAs), alongside increased lactate levels in acute DVT samples. Metabolomic profiles showed only partial normalization at follow-up, indicating persistent metabolic dysregulation. Overall, the reduced glucose metabolism and increased lactate levels indicate anaerobic metabolism, likely caused by tissue hypoxia due to impaired blood flow. Glutamine, essential for DNA, ATP, and protein synthesis, was notably reduced, potentially impairing endothelial cell proliferation and vascular repair. The presence of adhesion molecules in the follow-up group confirms persistent endothelial dysfunction. These findings suggest that metabolic and endothelial alterations may persist long after acute inflammation resolves in DVT patients. In conclusion, the persistence of metabolic dysregulation suggests chronic metabolic stress in these patients, potentially resulting from ongoing endothelial damage, low-grade inflammation, or altered mitochondrial function due to past tissue hypoxia. Full article

Previous studies suggested a certain efficiency of proteinogenic branched-chain amino acid (BCAA) and magnesium supplementations in reducing cardiovascular risk and increasing quality of life. This investigation assessed the anti-atherogenic and anti-calcific effects of BCAA (55 mg/day, corresponding to a human equivalent dose of 13.5 g/day) and magnesium citrate (MgCit, 1.85 mg/day, corresponding to a human equivalent dose of 450 mg/day) intake in male and female ApoE-knockout mice, with the treatment initiation at either 1, 3, or 6 months of age. At the 12-month time point, lipid retention and calcium deposition in the aortic valve, lipid burden in the aorta, and serum ionized calcium were evaluated. The early BCAA intake (from 1/3 to 12 months of age) significantly reduced lipid retention in the aortic valve, whilst MgCit decreased ionized calcium. Both of these protective effects were higher in male than in female mice. Furthermore, it was tested whether human serum albumin (HSA) or MgCit can be applied to decrease the serum calcification propensity in 100 patients with myocardial infarction. A dual supplementation with HSA and MgCit reduced serum calcification propensity in 68% of cases. Collectively, these results highlight the potential benefits of BCAA/HSA and magnesium supplementations for cardiovascular prevention and justify further clinical trials in this regard. Full article

Background: High-throughput metabolomics studies have promoted the discovery of candidate biomarkers linked to atherosclerosis (AS). This narrative systematic review summarises metabolomics studies conducted in (1) individuals with subclinical AS (assessed by imaging techniques such as carotid intimal media thickness, IMT, and coronary artery calcium, CAC), (2) patients with established atherosclerotic plaques, and (3) individuals with AS risk factors. Methods: The systematic search was conducted in the PubMed database according to the Preferred Reporting Items for Systematic Reviews and Meta-analysis (PRISMA) guidelines. The inclusion criteria were as follows: (i) publication date between 2009 and 2024; (ii) identification of potential biomarkers for AS in subjects with a diagnosis of AS or with one or more traits characteristic of the disease (i.e., CAC or IMT); (iii) identification of potential AS biomarkers in subjects with atherogenic clinical conditions (i.e., Down’s syndrome, DS, polycystic ovarian syndrome, PCOS, and systemic lupus erythematosus, SLE); (iv) metabolomic studies; and (iv) studies in human samples. Exclusion criteria comprised the following: (i) studies on lipid metabolic diseases unrelated to AS, (ii) “omics” results not derived from metabolomics, (iii) reviews and studies in animal models or cell cultures, and (iv) systematic reviews and meta-analyses. Of 90 eligible studies screened, 24 met the inclusion criteria. Results: Across subclinical and overt AS, consistent disturbances were observed in amino acid, lipid, and carbohydrate metabolism. Altered profiles included branched-chain amino acids (BCAAs), aromatic amino acids (AACs) and derivatives (e.g., kynurenine–tryptophan pathway), bile acids (BAs), androgenic steroids, short-chain fatty acids (FAs)/ketone intermediates (e.g., acetate, 3-hydroxybutyrate, 3-HB), and Krebs cycle intermediates (e.g., citrate). Several metabolites (e.g., glutamine, lactate, 3-HB, phosphatidylcholines, PCs/lysophosphatidylcholines, lyso-PCs) showed reproducible associations with vascular phenotypes (IMT/CAC) and/or clinical AS. Conclusions: The identification of low-weight metabolites altered in both subclinical and overt AS suggests their potential as candidate biomarkers for early AS diagnosis. Given the steady increase in deaths from cardiovascular disease, a manifestation of advanced AS, this finding could have significant clinical relevance. Full article

Anabolic resistance, consisting of a diminished ability of aging muscle to respond to anabolic stimuli such as exercise and protein intake, is a key contributor to age-related declines in muscle mass. However, diseases and lifestyle factors associated with aging, including insulin resistance states, overweight/obesity, persistent inflammation and specifically—as a focus herein—physical inactivity and inadequate dietary protein-intake habits, might interact with chronological impairments in muscle anabolism. In this context, master athletes, as individuals who have engaged in lifelong structured exercise, including regular training and sports participation, offer a valuable model for studying processes of chronological vs. inactivity-related aging. While these lifelong exercisers may present improved body composition parameters and other potential benefits in terms of muscle mass and function, it remains unclear whether exercise practice throughout life can prevent the development of anabolic resistance associated with aging. Albeit limited, evidence has indicated that even in lifelong-trained older individuals there is a blunted post-exercise muscle anabolic response compared to younger athletes. However, there is a paucity of data to systematically understand the differences in postprandial anabolic response to varying protein doses in older vs. young athletes. In lieu of the above, it seems reasonable that master athletes may benefit from increasing protein intake closer to the upper limit of current recommendations (1.6–2.0 g/kg/day). In addition, supplementing their diet with ingredients that have established anabolic potential, including branched chain amino acids (BCAAs) such as leucine, the leucine metabolite β-hydroxy-β-methylbutyrate (HMB), and n3-polyunsaturated fatty acids (n3-PUFA), may potentiate the anabolic response to protein and exercise. Full article

Background: β-lactoglobulin (BLG) is a protein found within whey protein (WP) that is rich in essential amino acids, most notably, leucine (LEU). LEU is considered the most potent EAA in the postprandial stimulation of muscle protein synthesis (MPS), such that suboptimal protein/essential amino acid (EAA) doses containing higher LEU content elicit muscle anabolism comparable to larger protein doses. Our objective was to test the effects of naturally LEU-rich BLG (~10 g protein) versus isonitrogenous whey protein isolate (WPI, ~10 g) on MPS. Methods: Ten healthy young men (26 ± 2 y; 179 ± 2 cm; 81 ± 3 kg) received BLG (1.57 g LEU) or WPI (1.02 g LEU) in a randomised double-blind cross-over fashion. A primed constant intravenous infusion of [1,2 ¹³C₂] LEU was used to determine MPS (isotope ratio mass spectrometry) at baseline and in response to feeding (FED) and feeding-plus-exercise (FED-EX; 6 × 8 unilateral leg extensions; 75% 1-RM). Plasma insulin and EAA’s were quantified. Results: Plasma EAA, branched-chain amino acid (BCAA), and LEU concentrations increased rapidly following both protein supplements but exhibited a significantly greater EAA/BCAA/leucinemia following BLG (p < 0.05 for all). MPS increased significantly in both FED (~52%) and FED-EX (~58%) states, with no significant differences between supplements. Conclusions: Both BLG and WPI effectively stimulated MPS doses in young healthy males, with BLG offering an advantage in EAA/BCAA/LEU bioavailability. It follows that future research should explore the potential of BLG in populations exhibiting anabolic resistance and exercise anabolism deficiency, such as older adults as well as frail and clinical populations, to assess its utility in preserving muscle mass under conditions of suboptimal protein intake. Full article

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

Background/Objectives: While many studies have explored the association between circulating branched-chain amino acids (BCAAs) and type 2 diabetes mellitus (T2DM), evidence on the prospective relationship between dietary BCAA intake and T2DM risk remains limited. We aimed to explore this relationship—both total and by dietary source—in a Mediterranean cohort. Methods: We used data from the SUN Project, a prospective and dynamic cohort of Spanish university graduates initiated in 1999. Dietary intake was assessed with a validated 136-item food frequency questionnaire at baseline and at 10 years. BCAA intake (valine, leucine, isoleucine) was estimated using the USDA amino acid database and adjusted for energy intake by the residual method. Participants were followed biennially through questionnaires to identify incident T2DM cases, confirmed by a supplementary questionnaire and medical report, following the ADA diagnostic criteria. Cox proportional hazards models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs), adjusting for potential confounders across four multivariable models. BCAA intake was modeled both categorically (tertiles) and continuously (per 0.5% energy or 5 g/day increase). Analyses were stratified by age and recruitment period. Results: After exclusions, 20,154 participants were included (mean follow-up: 14.67 ± 5.8 years), with 220 incident T2DM cases identified. For each 0.5% energy increment intake from BCAA, there was no association with T2DM (adjusted HR: 1.01; 95% CI: 0.69–1.20). Among men, the adjusted HR was 0.91, 95% CI: 0.69–1.20. Among women, it was 1.40, 95% CI: 0.94–2.09. In the overall cohort, higher BCAA intake showed a non-significant inverse association with the T2DM risk when comparing extreme tertiles (HR = 0.81; 95% CI: 0.48–1.37), which strengthened when repeated dietary measures were considered (HR = 0.70; 95% CI: 0.46–1.06, p-trend = 0.06). Analyses by BCAA sources (animal vs. plant) and stratified by sex, weight status, and age did not reveal consistent patterns, though exploratory findings suggested potential effect modification by sex and adiposity. Sensitivity analyses confirmed the lack of robust associations, with some subgroup-specific signals being limited by low event numbers and wide CIs. Conclusions: Given the power limitations and the modest, non-significant associations observed, these findings should be considered preliminary evidence that may help guide future research on the role of dietary BCAAs in glucose metabolism and diabetes risk. Full article