Search Results (98)

This study investigated the systemic metabolic effects of feeding a Fusarium-contaminated diet to early-lactation Holstein cows, with or without a mycotoxin-deactivating product (MDP; Mycofix^® Plus, BIOMIN Holding GmbH, Tulln, Austria). Thirty cows were divided into three dietary groups: a mildly contaminated control (CTR), a moderately contaminated diet containing zearalenone and deoxynivalenol (MTX), and the same contaminated diet supplemented with MDP. Plasma collected at 56 days in milk was analyzed by untargeted ultra-high-performance liquid chromatography (UHPLC) coupled with high-resolution mass spectrometry (HRMS), and multivariate models identified discriminant metabolites and pathways. MTX-fed cows showed alterations in sphingolipid metabolism, including accumulation of ceramide (t18:0/16:0), lactosylceramide, and sphinganine 1-phosphate, consistent with ceramide synthase inhibition and lipid remodeling stress. Increases in estradiol, estrone, and cholesterol sulfate suggested endocrine disruption, while elevated 8-oxo-dGMP indicated oxidative DNA damage. MDP supplementation mitigated these alterations, reducing sphingolipid intermediates, modulating tryptophan and glycerophospholipid pathways, and lowering oxidative stress markers. Metabolites such as riboflavin, pipecolic acid, and N-acetylserotonin could be likely associated with an improved mitochondrial function and redox homeostasis, although future studies are required to confirm this hypothesis. Additionally, MDP-fed cows exhibited distinct shifts in pyrimidine and nucleotide metabolism. Overall, MDP effectively counteracted Fusarium-related metabolic disturbances, supporting its protective role in maintaining lipid balance, hormonal stability, oxidative control, and metabolic resilience. Full article

Vascular calcification (VC) is a multifactorial pathological deposition of calcium in the vasculature and is associated with severe cardiovascular outcomes, particularly in patients with chronic kidney disease (CKD). Various vitamin K analogs have been found to influence the development of VC. We utilized a high-phosphate-induced VC model in mouse vascular smooth muscle cells (VSMCs) and developed an in vivo VC model using ApoE^−/− mice subjected to 5/6 nephrectomy and fed an oral high-phosphorus diet to evaluate the effect of the vitamin K3 analog phthiocol. Transdermal glomerular filtration rate measurement, pulse wave velocity for aortic stiffness assessment, blood biochemical analysis, and pathological examinations were conducted. Phthiocol suppressed reactive oxygen species production and reduced subsequent cell death and calcification in a dose-dependent manner. It inhibited osteogenic trans-differentiation by restoring the PI3K/Akt pathway, activating Nrf2/HO-1 antioxidation signaling, and downregulating IL-1β and TNF-α. The high-phosphate diet in ApoE^−/− CKD mice significantly induced dyslipidemia, renal impairment, hyperphosphatemia, aortic stiffness, and calcium deposition in aortic tissue compared to the control group. Phthiocol treatment markedly improved dyslipidemia, hyperphosphatemia, and aortic stiffness. The vitamin K3 analog phthiocol ameliorates phosphate-induced osteogenic trans-differentiation of VSMCs and subsequent VC by restoring the PI3K/Akt pathway and enhancing Nrf2/HO-1 antioxidant activity. Full article

Background/Objectives: It would be desirable to reduce the intake of inorganic phosphate (P), which is easily absorbed and is associated with cardiovascular disease. The phosphate-to-urea nitrogen ratio (P/UUN) in urine should reflect the proportion of inorganic P ingested relative to protein intake. In this manuscript, we will refer to this parameter as P/UUN, which is conceptually equivalent to the phosphate-to-urea ratio (P/U). These studies aim to evaluate whether an increased intake of inorganic P translates into an increase in the P/UUN. Methods: A total of 18 healthy volunteers (Study-1) and 18 chronic kidney disease patients (Study-2) were included. At baseline, all participants completed a 3-day dietary survey, and on the third day collected a 24 h urine sample. In Study-2, blood samples were also obtained. Participants were then stratified into three groups (6 per group) for a 3-day dietary intervention: control group: maintained their usual diet; soda group: consumed soda zero, a source of added inorganic P; and processed cheese group: consumed fresh processed cheese, which includes both organic and inorganic P additives. At last visit, all participants again completed a 3-day dietary survey and collected a 24 h urine sample (and blood samples in Study-2). Dietary P intake was estimated using two tools: the diet calibrator and the Spanish Food Composition Database (BEDCA). Results: After the intervention, neither BEDCA nor the diet calibrator was able to provide an accurate measurement of inorganic P ingested. However, only in the soda group, P/UUN increased in both studies (p = 0.046 and 0.047). In Study-2, the levels of FGF23 and klotho remained unchanged (p = 0.9 and p = 0.7, respectively). Conclusions: These findings suggest that urinary P/UUN ratio may be a useful biomarker to monitor changes in inorganic P intake and could help to individualize dietary recommendations to reduce inorganic P exposure without restricting protein intake. Full article

Aquaculture effluents rich in phosphorus and nitrogen (P and N) can lead to eutrophication of aquatic ecosystems. These nutrients may contribute to harmful algal blooms, oxygen depletion, and deterioration of water quality, which poses a threat to aquatic biodiversity. In shrimp diets, environmental impacts from P and N nutrient leaching can be reduced by improving dietary P digestibility through the use of alternative ingredients. While fishmeal, with its high phosphorus content, has traditionally been a primary source, its declining use due to cost and limited availability necessitates the inclusion of inorganic P sources to meet shrimp nutritional requirements. Optimising these sources ensures adequate phosphorus availability while minimising nutrient waste. This study evaluated the effects of inorganic phosphate supplementation (monoammonium phosphate, MAP; monosodium phosphate, MSP; and sodium calcium phosphate, SCP-2%) in standard diets (35% CP) on nutrient digestibility, residue generation, and performance of Litopenaeus vannamei. Results showed that phosphorus digestibility exceeded 96% across all phosphate sources, with MSP achieving the highest values. Calcium digestibility was notably higher in diets containing monocalcium phosphate, such as SCP-2%, which demonstrated superior digestibility values. No significant differences were observed in nitrogen or phosphorus excretion; however, residue analysis revealed that SCP-2% diets generated the lowest nitrogenous waste relative to ingested nitrogen, whereas MAP diets produced the highest nitrogen residues, followed by the Control diet. For phosphorus residues, the Control diet showed the greatest proportion relative to ingested phosphorus, followed by MSP. Phosphate inclusion did not affect shrimp growth, survival, or body composition. However, phosphorus and calcium retention efficiencies were inversely proportional to their dietary content, underscoring the importance of optimising phosphate sources to enhance nutrient utilisation and minimise environmental impact. Full article

Considering the importance of carotenoids in the human diet, their enhancement is a key trait in current breeding programs. This study assessed lutein, zeaxanthin, α-carotene, and β-carotene levels in the flesh of mature fruits from 257 global C. pepo accessions. Lutein and β-carotene were the most prevalent, with top accessions identified for each carotenoid. A panel of 120 accessions with reliable carotenoid contents and genetic diversity was analyzed using 23,111 GBS-generated SNPs in genome-wide association studies (GWAS). Three genomic regions (qtl1, qtl3, and qtl13) on chromosomes 1, 3, and 13 were significantly linked to carotenoid levels, with alternative alleles increasing the carotenoid content, leading to yellowish–orange flesh. Seven candidate genes were identified: CpTIC56, CpHSHP70, and CpPDL8, which regulate carotenoid biosynthesis in chloroplasts; CpSPX and CpPHO1, associated with phosphate homeostasis and carotenoid buildup; CpMYB106, co-expressed with carotenoid biosynthesis genes; and a CpPPR RNA-binding protein. RNA-seq data from yellow- and white-fleshed fruits supported their involvement in carotenoid accumulation. These results improve our understanding of the genetic control of carotenoid buildup in C. pepo fruit, supporting breeding efforts for improved nutritional quality. Full article

Previous work has shown that mouse models fed a non-obesogenic high-fat diet have preserved cardiac function and no obesity-associated comorbidities such as diabetes. However, they do suffer increased cardiac vulnerability to ischemic reperfusion (I/R) injury, which has been attributed to changes in Ca²⁺ handling, oxidative stress, and mitochondrial transition pore activity. However, there have been no studies investigating the involvement of metabolites. Wild-type mice were fed either a control or a non-obesogenic high-fat diet for ~26 weeks. Key cardiac metabolites were extracted from freshly excised hearts and from hearts exposed to 30 min global ischemia followed by 45 min reperfusion. The extracted metabolites were measured using commercially available kits and HPLC. Hemodynamic cardiac function was monitored in Langendorff perfused hearts. Levels of energy-rich phosphates and related metabolites were similar for both hearts fed a control or a high-fat diet. However, the high-fat diet decreased cardiac glycogen and increased cardiac lactate, hypoxanthine, alanine, and taurine levels. Langendorff perfused hearts from the high-fat diet group suffered more ischemic stress during ischemia, as shown by the significantly shorter time needed for onset and for reaching maximal ischemic (rigor) contracture. Following I/R, there was a significant decrease in myocardial adenine nucleotides and a significant increase in the levels of alanine and purines for both groups. Most of the principal amino acids tended to fall during I/R. Hearts from mice fed a high-fat diet showed more changes during I/R in markers of energetics (phosphorylation potential and energy charge), metabolic stress (lactate), and osmotic stress (taurine). This study suggests that cardiac metabolic changes due to high-fat diet feeding, independent of obesity-related comorbidities, are responsible for the marked metabolic changes and the increased vulnerability to I/R. Full article

Background: Type 2 diabetes (T2D), the most common form of diabetes, is associated with a significantly elevated risk of cardiovascular and cerebrovascular complications. However, circulating metabolic signatures that reliably predict the transition to insulin resistance, and are potentially linked to increased vascular risk, remain incompletely characterized. Rodent models, particularly those induced by a high-fat diet (HFD) combined with low-dose streptozotocin (STZ), are widely used to study the progression of T2D. However, the systemic metabolic shifts associated with this model, especially at the plasma level, are poorly defined. Methods: In this study, we performed untargeted liquid chromatography–mass spectrometry (LC-MS)-based metabolomic profiling on plasma samples from control, HFD-only (obese, insulin-sensitive), and HFD + STZ (obese, insulin-resistant) C57BL/6 mice. Results: In the HFD + STZ cohort, plasma profiles showed a global shift toward lipid classes; depletion of aromatic and branched-chain amino acids (BCAAs); accumulation of phenylalanine-derived co-metabolites, consistent with gut–liver axis dysregulation; elevations in glucose, fructose-6-phosphate, and nucleoside catabolites, indicating impaired glucose handling and heightened nucleotide turnover; increased free fatty acids, reflecting membrane remodeling and lipotoxic stress; and higher cAMP, thyroxine, hydrocortisone, and uric acid, consistent with endocrine and redox imbalance. By contrast, HFD-only mice exhibited elevations in aromatic amino acids and BCAAs relative to controls, a pattern compatible with early obesity-associated adaptation while insulin signaling remained partially preserved. KEGG analysis revealed disturbances in carbohydrate metabolism, amino acid degradation, nucleotide turnover, and hormone-related pathways, and HMDB mapping linked these changes to T2D, obesity, heart failure, and renal dysfunction. Conclusion: Collectively, these findings delineate insulin resistance-specific plasma signatures of metabolic inflexibility and inflammatory stress in the HFD + STZ model, distinguishing it from HFD alone and supporting its utility for mechanistic studies and biomarker discovery. Importantly, this plasma metabolomics study shows that insulin-sensitive and insulin-resistant states exhibit distinct variation in circulating metabolites and cardiovascular risk factors, underscoring the translational value of plasma profiling. Full article

This study evaluated the physicochemical and morphological properties of tooth enamel in patients with caries-predisposing SNPs (rs4694075 in AMBN and rs2337359 in TUFT1 genes), based on the DMFT index. We included 40 of 120 individuals (aged 19–43), collecting stimulated saliva and 58 healthy teeth extracted for orthodontic/surgical reasons. Saliva DNA was genotyped. Enamel properties were assessed using Vickers microhardness, deposition thickness, and calcium content. Genotype and allele frequencies aligned with the literature. The TUFT1C/C genotype subgroup showed a significantly higher DMFT index (p = 0.03) compared to the T/T genotype, while AMBN showed no such correlation. Calcium content, microhardness, and enamel thickness were similar across all polymorphic variants of both genes. A statistically significant correlation (p = 0.003) was found between reduced enamel calcium content and a higher DMFT index. Despite existing literature on the subject, the studied SNPs did not reflect any correlation with morphological or physicochemical changes in enamel. The above results suggest that genetic variability identifies patients classified by dentists as being at higher risk of caries, even though these patients follow a non-cariogenic diet and adhere to a hygiene regime. As no structural or physicochemical changes in the enamel of this group were observed, the potential cause may be disturbances in the remineralisation mechanisms or enamel surface properties that promote biofilm adhesion in polymorphic patients. Intensive tooth calcification control algorithms using LIF and RVG, as well as remineralisation cycles to increase hydroxyapatite saturation with calcium phosphates and bioadhesive fluoride delivery systems for long-term biofilm control, are used to more effectively prevent or slow down the progression of caries. Full article

Phosphorus is one of the most abundant minerals in the body and plays a critical role in numerous cellular and metabolic processes. Most of the phosphate is deposited in bones, 14% is present in soft tissues as various organic phosphates, and only 1% is found in extracellular space, mainly as inorganic phosphate. The plasma inorganic phosphate concentration is closely maintained between 2.5 and 4.5 mg/dL by intertwined interactions between fibroblast growth factor 23 (FGF-23), parathyroid hormone (PTH), and vitamin D, which tightly regulate the phosphate trafficking across the gastrointestinal tract, kidneys, and bones. Disruption of the strict hemostatic control of phosphate balance can lead to altered cellular and organ functions that are associated with high morbidity and mortality. In the past three decades, there has been a steady increase in the prevalence of kidney failure (KF) among populations. Individuals with KF have unacceptably high mortality, and well over half of deaths are related to cardiovascular disease. Abnormal phosphate metabolism is one of the major factors that is independently associated with vascular calcification and cardiovascular mortality in KF. In early stages of CKD, adaptive processes involving FGF-23, PTH, and vitamin D occur in response to dietary phosphate load to maintain plasma phosphate level in the normal range. However, as the CKD progresses, these adaptive events are unable to overcome phosphate retention from continued dietary phosphate intake and overt hyperphosphatemia ensues. As these hormonal imbalances and the associated adverse consequences are driven by the underlying hyperphosphatemic state in KF, it appears logical to strictly control serum phosphate. Conventional dialysis is inadequate in removing phosphate and most patients require dietary restrictions and pharmacologic interventions to manage hyperphosphatemia. However, diet control comes with many challenges with adherence and may place patients at risk for inadequate protein intake and malnutrition. Phosphate binders help to reduce phosphate levels but come with a sizable pill burden and high financial costs and are associated with poor adherence and psychosocial issues. Additionally, long-term use of binders may increase the risk of calcium, lanthanum, or iron overload or promote gastrointestinal side effects that exacerbate malnutrition and affect quality of life. Given the aforesaid challenges with phosphorus binders, novel therapies targeting small intestinal phosphate absorption pathways have been investigated. Recently, tenapanor, an agent that blocks paracellular absorption of phosphate via inhibition of enteric sodium–hydrogen exchanger-3 (NHE3) was approved for the treatment of hyperphosphatemia in KF. While various clinical tools are now available to manage hyperphosphatemia, there is a lack of convincing clinical data to demonstrate improvement in outcomes in KF with the lowering of phosphorus level. Conceivably, deleterious effects associated with hyperphosphatemia could be attributable to disruptions in phosphorus-sensing mechanisms and hormonal imbalance thereof. Further exploration of mechanisms that precisely control phosphorus sensing and regulation may facilitate development of strategies to diminish the deleterious effects of phosphorus load and improve overall outcomes in KF. Full article

This study investigates the effect of dietary Lactobacillus plantarum supplementation on juvenile coho salmon (Oncorhynchus kisutch). Four groups of the juveniles (initial weight 103.87 ± 2.65 g) were fed for 10 weeks with four diets containing 0 (control diet), 10⁵ (T1), 10⁷ (T2), and 10⁹ (T3) cfu/g of L. plantarum. The main results are as follows: Compared with the control diet, the final weight, specific growth rate (SGR), and weight gain rate (WGR) of the juveniles fed the T1, T2, and T3 diet significantly (p < 0.05) increased, while the feed coefficient ratio (FCR) expressed an opposite trend. The activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-PX) in the serum of the juveniles fed the T2 diet significantly (p < 0.05) increased, while the malondialdehyde (MDA) expressed an opposite trend. The expression of phosphatidylinositol 4,5-bisphosphate 3-kinase (pi3k), AKT-interacting protein (akt), mechanistic target of rapamycin kinase (mtor), glucose-6-phosphate dehydrogenase (g6pd), sod, cat, and gsh-px genes in the liver of the juveniles fed the T2 diet significantly (p < 0.05) increased. In conclusion, the T2 diet significantly improved the growth performance, antioxidant capacity, and upregulated key mTOR pathway genes in juvenile coho salmon. Full article

The increasing global population and the environmental consequences of meat consumption have led to the exploration of alternative sources of protein. Edible insects have gained attention as a sustainable and nutritionally rich meat alternative. We investigated the effects of two commonly consumed insects, Protaetia brevitarsis seulensis larva and Bombyx mori pupa, on beneficial gut microbiota growth, using whole 16s metagenome sequencing to assess diet-associated changes. Seven-week-old female C57BL/6J mice were administered the edible insects, along with fracto-oligosaccharide (FOS) as a positive control and sham (phosphate buffer saline (PBS)) as a negative control, to assess the relative abundance of insect-diet-associated gut microbes. In total, 567 genera and 470 species were observed, and among these, 15 bacterial genera were differentially abundant in all three groups. These results show that among the two insects, Bombyx mori pupa polysaccharides have a greater ability to regulate beneficial probiotics and next-generation probiotics. In particular, Lactococcus garvieae, which has promising effects on the gastrointestinal tracts of humans and animals, was significantly enriched in both Protaetia brevitarsis seulensis larva and Bombyx mori pupa polysaccharides, similar to fracto-oligosaccharide. The results suggest that the consumption of these insects, particularly polysaccharides, can enhance the growth of beneficial gut microbes, potentially leading to improved overall health in healthy populations. Full article

This study aimed to explore the effects of sodium butyrate on liver metabolism in goats subjected to a high-concentrate diet. We randomly assigned twelve Saanen-lactating goats into two groups, one of which received a high-concentrate diet (concentrate: forage = 60:40, control group), while the other received the same basal diet supplemented with sodium butyrate (SB) (10 g/kg basal diet, SB group). Compared with the control diet, the SB diet considerably increased the milk fat percentage and content (p < 0.05), with an increase of 0.67% in the milk fat content of the SB group. By employing a global metabolomics approach based on ultra-performance liquid chromatography–tandem mass spectrometry (UPLC–MS/MS), we identified 6748 ions in ESI+ mode and 3573 ions in ESI− mode after liver isolation from both groups. A total of twenty-three metabolites, including phospholipids, fatty acids, and ribose phosphate, were found to be dysregulated according to a search against the human metabolome database (HMDB). Pathway analysis revealed activation of the pentose phosphate pathway, glycerophospholipid metabolism, and unsaturated fatty acid synthesis. The SB diet also modulated the expression of key lipogenic enzymes, such as acetyl-CoA carboxylase (ACC) and stearoyl-CoA desaturase (SCD-1), which are downstream targets of the transcription factor sterol regulatory element-binding proteins-1c (SREBP-1c), inducing a significant upregulation (p < 0.05). Furthermore, 6-phosphogluconate dehydrogenase (6PGDH) levels in the liver were elevated after the lactating goats were fed the SB diet (p < 0.05). Our study reveals that the SB diet may offer substantial benefits in enhancing the milk quality of subacute ruminal acidosis (SARA) goats. This is accomplished by augmenting the activity of the liver pentose phosphate pathway and the process of de novo fatty acid synthesis in lactating goats. Full article

Both maternal obesity and postnatal consumption of obesogenic diets contribute to the development of metabolic dysfunction-associated steatotic liver disease (MASLD) and hepatocellular carcinoma (HCC). However, there is no consensus as to whether diets that are high in fat or carbohydrates/sugars differentially influence the development of HCC. Moreover, the long-term effects of prenatal HF exposure on HCC and whether this is influenced by postnatal diet has not yet been evaluated. C57BL/6 dams were fed either a low-fat, high-carbohydrate control (C) or low-carbohydrate, high-fat (HF) diet. At weaning, male and female offspring were fed the C or HF diet, generating four diet groups: C/C, C/HF, HF/C and HF/HF. Tissues were collected at 16 months of age and livers were assessed for MASLD and HCC. Glucose regulation and pancreatic morphology were also evaluated. Liver tissues were assessed for markers of glycolysis and fatty acid metabolism and validated using a human HCC bioinformatic database. Both C/HF and HF/HF mice developed obesity, hyperinsulinemia and a greater degree of MASLD than C/C and HF/C offspring. However, despite significant liver and pancreas pathology, C/HF mice had the lowest incidence of HCC while tumour burden was highest in HF/C male offspring. The molecular profile of HCC mouse samples suggested an upregulation of the pentose phosphate pathway and a downregulation of fatty acid synthesis and oxidation, which was largely validated in the human dataset. Both pre-weaning HF diet exposure and post-weaning consumption of a high-carbohydrate diet increased the risk of developing spontaneous HCC in aged mice. However, the influence of pre-weaning HF feeding on HCC development appeared to be stronger in the context of post-weaning obesity. As rates of maternal obesity continue to rise, this has implications for the future incidence of HCC and possible dietary manipulation of offspring carbohydrate intake to counteract this risk. Full article

Dietary restriction (DR) protocols frequently employ intermittent fasting. Following a period of fasting, meal consumption increases lipogenic gene expression, including that of NADPH-generating enzymes that fuel lipogenesis in white adipose tissue (WAT) through the induction of transcriptional regulators SREBP-1c and CHREBP. SREBP-1c knockout mice, unlike controls, did not show an extended lifespan on the DR diet. WAT cytoplasmic NADPH is generated by both malic enzyme 1 (ME1) and the pentose phosphate pathway (PPP), while liver cytoplasmic NADPH is primarily synthesized by folate cycle enzymes provided one-carbon units through serine catabolism. During the daily fasting period of the DR diet, fatty acids are released from WAT and are transported to peripheral tissues, where they are used for beta-oxidation and for phospholipid and lipid droplet synthesis, where monounsaturated fatty acids (MUFAs) may activate Nrf1 and inhibit ferroptosis to promote longevity. Decreased WAT NADPH from PPP gene knockout stimulated the browning of WAT and protected from a high-fat diet, while high levels of NADPH-generating enzymes in WAT and macrophages are linked to obesity. But oscillations in WAT [NADPH]/[NADP⁺] from feeding and fasting cycles may play an important role in maintaining metabolic plasticity to drive longevity. Studies measuring the WAT malate/pyruvate as a proxy for the cytoplasmic [NADPH]/[NADP⁺], as well as studies using fluorescent biosensors expressed in the WAT of animal models to monitor the changes in cytoplasmic [NADPH]/[NADP⁺], are needed during ad libitum and DR diets to determine the changes that are associated with longevity. Full article

To investigate the activities of intestinal digestive enzymes, liver antioxidant enzymes, immunological enzymes, and glucometabolic enzymes in largemouth bass (Micropterus salmoides) under the biofloc model, an experiment was conducted in 300-liter glass tanks. The experiment comprised a control group, which was fed a basal diet, and a biofloc group, where glucose was added to maintain a C/N ratio of 15. Each group had three parallel setups, with a stocking density of 20 fish per tank. The experiment ran for 60 days, employing a zero-water exchange aquaculture model. The results showed that at the end of the culture period, there were no significant differences between the initial weight, final weight, WGR, SGR, and SR of the biofloc group and the control group of largemouth bass (p > 0.05), whereas the lower FCR and the higher PER in the biofloc group were significant (p < 0.05); intestinal α-amylase, trypsin, and lipase activities of largemouth bass in the biofloc group were significantly increased by 37.20%, 64.11%, and 51.69%, respectively, compared with the control group (p < 0.05); liver superoxide dismutase and catalase activities, and total antioxidant capacity of largemouth bass in the biofloc group were significantly increased by 49.26%, 46.87%, and 98.94% (p < 0.05), while the malondialdehyde content was significantly reduced by 19.91% (p < 0.05); liver lysozyme, alkaline phosphatase, and acid phosphatase activities of largemouth bass in the biofloc group were significantly increased by 62.66%, 41.22%, and 29.66%, respectively (p < 0.05); liver glucokinase, pyruvate kinase, glucose-6-phosphate kinase, pyruvate kinase, glucose-6-phosphatase, and glycogen synthase activities were significantly increased by 46.29%, 99.33%, 32.54%, and 26.89%, respectively (p < 0.05). The study showed that the biofloc model of culturing largemouth bass can not only enhance digestive enzyme activities, antioxidant capacity, and immune response but can also promote the process of glucose metabolism and reduce feeding costs. This study provides data support for healthy culturing of largemouth bass in future production, provides a theoretical reference for optimizing the biofloc technology culture model, and is crucial for promoting the healthy and green development of aquaculture. Full article