Search Results (65)

Lichens, symbiotic organisms with a high tolerance to harsh environments, possess a greater diversity of sterols than other organisms. Sterols are involved in maintaining membrane integrity, hormone biosynthesis, and signal transduction. (1) Background: A characteristic feature of lichen sterols is a high degree of unsaturation, which influences membrane properties. Desaturases play an important role in the synthesis of unsaturated sterols, in particular, sterol C-5 desaturase (ERG3), which controls the conversion of episterol to ergosterol. Earlier, we demonstrated that the treatment of the lichen Peltigera canina with low and elevated temperatures results in changes in the levels of episterol and ergosterol. (2) Methods: Here, for the first time, we identified ERG3 in P. canina and, using an in silico analysis, we showed that PcERG3 belongs to the superfamily of fatty acid hydrolyases. A phylogenetic analysis was conducted to determine the evolutionary relationships of PcERG3. (3) Results: A phylogenetic analysis showed that PcERG3 clusters with ERG3 from other Peltigeralian and non-Peltigeralian lichens and also with ERG3 from free-living fungi. This suggests that PcERG3 has an ancient evolutionary origin and is related to fungi with lichenized ancestors, e.g., Penicillium. The differential expression of PcERG3 in response to temperature stress, a dehydration/rehydration cycle, and heavy metal exposure suggests that it plays a crucial role in maintaining the balance between more and less saturated sterols and, more generally, in membrane functioning. The multifaceted response of P. canina to abiotic stresses was documented by simultaneously measuring changes in the expression of PcERG3, as well as the genes encoding the heat shock proteins, PcHSP20 and PcHSP98, and PcSOD1, which encodes the antioxidant enzyme superoxide dismutase. (4) Conclusions: These findings suggest that PcERG3 is similar to the sterol C-5 desaturases from related and free-living fungi and plays important roles in the molecular mechanisms underlying the tolerance of lichens to environmental stress. Full article

Inflammatory bowel disease is a risk factor for brain dysfunction; however, the underlying mechanisms remain largely unknown. In this study, we aimed to explore the potential molecular mechanisms through which intestinal inflammation affects brain function and to verify these mechanisms. Mice were treated with multiple cycles of 1% w/v dextran sulfate sodium (DSS) in drinking water to establish a chronic colitis model. Behavioral tests were conducted using the open field test (OFT), tail suspension test (TST), forced swimming test (FST), and Morris water maze test (MWM). Brain metabolomics, transcriptomics, and proteomics analyses were performed, and key target proteins were verified using qPCR and immunofluorescence. Four cycles of DSS administration induced colitis, anxiety, depression, and spatial memory impairment. The integrated multi-omics characterization of colitis revealed decreased brain chenodeoxycholic acid (CDCA) levels as well as reduced stearoyl-CoA desaturase (Scd1) gene and protein expression. Transplantation of the colitis microbiome resulted in anxiety, depression, impaired spatial memory, reduced CDCA content, decreased Scd1 gene and protein expression, and lower concentrations of monounsaturated fatty acids (MUFAs), palmitoleate (C16:1), and oleate (C18:1) in the brain. In addition, CDCA supplementation improved DSS-induced colitis, alleviated depression and spatial memory impairment, and increased Scd1 gene and protein expression as well as MUFA levels in the brain. The gut microbiome induced by colitis contributes to neurological dysfunction, possibly through the CDCA–Scd1 signaling axis. CDCA supplementation alleviates colitis and depressive behavior, likely by increasing Scd1 expression in the brain. Full article

This experiment was arranged to explore the impacts of dietary MHA on liver lipid metabolism in largemouth bass. A total of 480 fish (14.49 ± 0.13 g) were randomly allocated into four groups, each with three replicates. They were then given four different diets containing graded levels of MHA (0.0, 3.0, 6.0, and 9.0 g/kg) for 84 days. The results showed that dietary MHA increased hepatic lipid vacuoles and lipid content (p < 0.05). Dietary supplementation with MHA 9.0 g/kg diets increased the activities of acetyl-coA carboxylase (ACC), fatty acid synthase (FAS), and stearoyl-coA desaturase 1 (SCD-1). Dietary MHA up-regulated the mRNA expressions of liver lipid synthesis (ACC, FAS, SCD-1 and SREBP-1c) (p < 0.05). Furthermore, compared with the 0.0 g/kg diet group, the group supplemented with 9.0 g/kg MHA in the diet exhibited a significant decrease in the activities of liver lipid-oxidation-related enzymes (acetyl-CoA carboxylase (ACC), fatty acid synthase (FAS), and stearoyl-CoA desaturase 1 (SCD-1), as well as HSL and CPT1) and the gene expressions of ATGL, HSLa, HSLb, CPT1a, and PPARα (p < 0.05). Additionally, the mRNA expressions and protein levels of SIRT1 and AMPK in the 9.0 g/kg MHA-supplemented group were significantly lower than those in the 0.0 g/kg diet group (p < 0.05). Overall, the present results suggested that dietary MHA could increase lipid accumulation through regulating SIRT1/AMPK signaling pathways in the livers of largemouth bass. Full article

Dietary interventions with food-derived natural products have emerged as a promising strategy to alleviate obesity. This study aims to investigate the anti-obesity effect of Hericium erinaceus protein (HEP) and its underlying mechanism. Our results demonstrated that HEP exhibited excellent radical scavenging activity in vitro. In vivo, HEP intervention reduced pancreatic lipase activity in the intestine and enhanced fat excretion, thereby inhibiting the absorption of dietary fats. Meanwhile, HEP ameliorated the body weight and organ indexes, dyslipidemia, insulin resistance, hepatic steatosis, and liver oxidative stress injuries in obese mice. The results of real-time PCR (qRT-PCR) and Western blot analyses indicated that HEP upregulated the expression of peroxisome proliferator-activated receptor α (PPARα), subsequently upregulated the expression of liver fatty acid oxidation-related genes (lipoprotein lipase (LPL), carnitine palmitoyltransferase 1a (CPT-1a), and acyl-CoA oxidase 1 (ACOX1)) and downregulated the expression of lipogenesis-related genes (sterol regulatory element-binding protein-1c (SREBP-1c), stearoyl-coenzyme A desaturase 1 (SCD-1), and fatty acid synthase (FASN)), thereby ameliorating lipid metabolism disorders. Therefore, these findings demonstrated that HEP exerted protective effects on lipid metabolism disorders by activating the PPARα pathway, indicating its potential as a dietary supplement for the prevention and amelioration of obesity. Full article

Background/Objectives: Obesity is a key factor in metabolic syndrome (MetS) development. Consumption of a high-fat diet (HFD) accelerates the onset of obesity and associated metabolic complications. Protaetia brevitarsis (PB) has been traditionally utilized in Korean medicine for its antioxidant, anti-diabetic, anticancer, and hepatoprotective effects. However, specific effects of PB hydrolysate on skeletal muscles have not been fully elucidated. Therefore, this study sought to assess the influence of PB on HFD-induced MetS, focusing on the lipid metabolism and inflammatory responses mediated by AMP-activated protein kinase activation. Methods: To induce obesity, 6-week-old C57BL/6J mice were maintained on an HFD for 8 weeks, after which PB hydrolysate was orally administered for 16 weeks while the HFD regimen was sustained. A glucose tolerance test was conducted orally to evaluate glucose regulation, and forelimb grip strength was assessed upon completion of the experimental period. Histological assessments, serum biochemical analysis, lipid extraction, Western blot analysis, and quantitative reverse-transcription polymerase chain reaction (qRT-PCR) were performed following euthanasia. Results: PB significantly reduced ectopic lipid deposition in skeletal muscles, enhanced muscle strength, and improved insulin sensitivity by increasing fatty acid oxidation via AMP-activated protein kinase/carnitine palmitoyltransferase 1 activation and inhibiting lipogenesis via stearoyl-CoA desaturase 1 gene downregulation. Furthermore, PB alleviated HFD-induced low-grade chronic inflammation by decreasing systemic monocyte chemoattractant protein 1 levels, thereby reducing ectopic fat deposition. Conclusions: This study highlights the potential of PB as a nutraceutical to mitigate MetS in HFD-fed mice. Full article

(1) Background: Odd-chain fatty acids (OCFAs) have garnered attention for their potential health benefits and unique roles in various biochemical pathways. Yarrowia lipolytica, a versatile yeast species, is increasingly studied for its capability to produce OCFAs under controlled genetic and environmental conditions. However, optimizing the synthesis of specific OCFAs, such as cis-9-heptadecenoic acid (C17:1), remains a challenge. (2) Methods: The gene coding for the Δ9 fatty acid desaturase, YlOLE1, and the gene coding the diacylglycerol O-acyltransferase 2, YlDGA2, were overexpressed in Y. lipolytica. With the engineered strain, the main goal was to fine-tune the production of OCFA-enriched lipids by optimizing the concentrations of sodium propionate and sodium acetate used as precursors for synthesizing odd- and even-chain fatty acids, respectively. (3) Results: In the strain overexpressing only YlDGA2, no significant changes in fatty acid composition or lipid content were observed compared to the control strain. However, in the strain overexpressing both genes, while no significant changes in lipid content were noted, a significant increase was observed in OCFA content. The optimal conditions for maximizing the cell density and the C17:1 content in lipids were found to be 2.23 g/L of sodium propionate and 17.48 g/L of sodium acetate. These conditions resulted in a cell density (optical density at 600 nm) of 19.5 ± 0.46 and a C17:1 content of 45.56% ± 1.29 in the culture medium after 168 h of fermentation. (4) Conclusions: By overexpressing the YlOLE1 gene and optimizing the concentrations of fatty acid precursors, it was possible to increase the content of OCFAs, mainly C17:1, in lipids synthesized by Y. lipolytica. Full article

The olive fruit is a drupe whose development and ripening takes several months from flowering to full maturation. During this period, several biochemical and physiological changes occur that affect the skin color, texture, composition, and size of the mesocarp. The final result is a fruit rich in fatty acids, phenolic compounds, tocopherols, pigments, sterols, terpenoids, and other compounds of nutritional interest. In this work, a transcriptomic analysis was performed using flowers (T0) and mesocarp tissue at seven different stages during olive fruit development and ripening (T1–T7) of the ‘Picual’ cultivar. A total of 1755 genes overexpressed at any time with respect to the flowering stage were further analyzed. These genes were grouped into eight clusters based on their expression profile. The gene enrichment analysis revealed the most relevant biological process of every cluster. Highlighting the important role of hormones at very early stages of fruit development (T1, Cluster 1), whereas genes involved in fatty acid biosynthesis were relevant throughout the fruit developmental process. Hence, genes coding for different fatty acid desaturase (SAD, FAD2, FAD3, FAD4, FAD5, FAD6, and FAD7) enzymes received special attention. In particular, 26 genes coding for different fatty acid desaturase enzymes were identified in the ‘Picual’ genome, contributing to the improvement of the genome annotation. The expression pattern of these genes during fruit development corroborated their role in determining fatty acid composition. Full article

In this study, the influence of fasting on hepatic glucose and lipid metabolism was explored by examining biochemical, antioxidative, and morphological indicators and transcriptional expression in the liver of javelin goby (Synechogobius hasta) after 0, 3, 7, or 14 days of starvation. Marked reductions in hepatic glycogen and triglycerides occurred from the seventh day of starvation until the end of the trial (p < 0.05). However, no alterations in hepatic cholesterol or protein were detected throughout the entire experiment (p > 0.05). During fasting, the activities of pyruvate kinase, lactate dehydrogenase, and glycogen phosphorylase a all rose firstly and then fell (p < 0.05). The activities of hepatic fatty acid synthase and acetyl-CoA carboxylase were minimized to their lowest levels at the end of food deprivation (p < 0.05), while lipase was elevated after 7–14 days of fasting (p < 0.05). Catalase, glutathione, and the total antioxidative capacity were increased and maintained their higher values in the later stage of fasting (p < 0.05), whereas malondialdehyde was not significantly changed (p > 0.05). Hepatic vein congestion, remarkable cytoplasmic vacuoles, and irregular cell shape were present in S. hasta which endured 3–7 days of fasting and were less pronounced when food shortage was prolonged. In terms of genes associated with glucose and lipid metabolism, the hepatic phosphofructokinase gene was constantly up-regulated during fasting (p < 0.05). However, the mRNA levels of glycogen synthase and glucose-6-phosphatase were obviously lower when the food scarcity extended to 7 days or more (p < 0.05). Fatty acid synthase, stearoyl-CoA desaturase 1, and peroxisome proliferator-activated receptor γ were substantially down-regulated in S. hasta livers after 7–14 days of food deprivation (p < 0.05). However, genes involved in lipolysis and fatty acid transport were transcriptionally enhanced to varying extents and peaked at the end of fasting (p < 0.05). Overall, starvation lasting 7 days or more could concurrently mobilize hepatic carbohydrates and fat as energy resources and diminished their hepatic accumulation by suppressing biosynthesis and enhancing catabolism and transport, ultimately metabolically and structurally perturbing the liver in S. hasta. This work presents preliminary data on the dynamic characteristics of hepatic glucose and lipid metabolism in S. hasta in response to starvation, which may shed light on the sophisticated mechanisms of energetic homeostasis in fish facing nutrient unavailability and may benefit the utilization/conservation of S. hasta. Full article

Background/Objectives: Stearoyl-coenzyme A desaturase 1 (SCD1) plays a crucial role in fatty acid metabolism. However, its roles in the feeding habit transformation of mandarin fish (Siniperca chuatsi) remain largely unknown. Methods: Juvenile mandarin fish (10.37 ± 0.54)g were trained to feed on an artificial diet and then divided into artificial diet feeders and nonfeeders according to their feed preference. Afterwards, the scd1 gene of mandarin fish (Sc-scd1) was identified and characterized, and its transcription difference was determined between S. chuatsi fed live artificial diets and those fed prey fish. Results: Our results show that Sc-scd1 coding sequence is 1002 bp long, encoding 333 amino acids. The assumed Sc-SCD1 protein lacks a signal peptide, and it contains 1 N-linked glycosylation site, 24 phosphorylation sites, 4 transmembrane structures, and 3 conserved histidine elements. We found that Sc-SCD1 exhibits a high similarity with its counterparts in other fish by multiple alignments and phylogenetic analysis. The expression level of Sc-scd1 was detected with different expression levels in all tested tissues between male and female individuals fed either live prey fish or artificial diets. Conclusions: In particular, the Sc-scd1 expression level was the highest in the liver of both male and female mandarin fish fed artificial diets, indicating that scd1 genes may be associated with feed adaption of mandarin fish. Taken together, our findings offer novel perspectives on the potential roles of scd1 in specific domestication, and they provide valuable genetic information on feeding habits for the domestication of mandarin fish. Full article

In order to study the effects of soybean isoflavones on the growth performance and lipid metabolism of juvenile Chinese mitten crabs, six experimental diets were formulated by gradient supplementation with 0%, 0.004% and 0.008% soybean isoflavones at different dietary lipid levels (10% and 15%). The groups were named as follows: NF-0 group (10% fat and 0% SIFs), NF-0.004 group (10% fat and 0.004% SIFs), NF-0.008 group (10% fat and 0.008% SIFs), HF-0 group (15% fat and 0% SIFs), HF-0.004 group (15% fat and 0.004% SIFs) and HF-0.008 group (15% fat and 0.008% SIFs). All crabs with an initial weight of 0.4 ± 0.03 g were fed for 8 weeks. The results showed that dietary supplementation with 0.004% or 0.008% SIFs significantly increased the weight gain and specific growth rate of crabs. Diets supplemented with 0.004% or 0.008% SIFs significantly reduced the content of non-esterified free fatty acids and triglycerides in the hepatopancreas of crabs at the 10% dietary lipid level. Dietary SIFs significantly decreased the relative mRNA expressions of elongase of very-long-chain fatty acids 6 (elovl6), triglyceride lipase (tgl), sterol regulatory element-binding protein 1 (srebp-1), carnitine palmitoyltransferase-1a (cpt-1a), fatty acid transporter protein 4 (fatp4), carnitine palmitoyltransferase-2 (cpt-2), Δ9 fatty acyl desaturase (Δ9 fad), carnitine palmitoyltransferase-1b (cpt-1b), fatty acid-binding protein 10 (fabp10) and microsomal triglyceride transfer protein (mttp) in the hepatopancreas of crabs. At the 15% dietary lipid level, 0.008% SIFs significantly increased the relative mRNA expressions of fatty acid-binding protein 3 (fabp3), carnitine acetyltransferase (caat), fatp4, fabp10, tgl, cpt-1a, cpt-1b and cpt-2 and significantly down-regulated the relative mRNA expressions of Δ9 fad and srebp-1. In conclusion, SIFs can improve the growth and utilization of a high-fat diet by inhibiting genes related to lipid synthesis and promoting lipid decomposition in juvenile Chinese mitten crabs. Full article

Background: High-fat diets cause gut dysbiosis and promote triglyceride accumulation, obesity, gut permeability changes, inflammation, and insulin resistance. Both cocoa butter and fish oil are considered to be a part of healthy diets. However, their differential effects on gut microbiome perturbations in mice fed high concentrations of these fats, in the absence of sucrose, remains to be elucidated. The aim of the study was to test whether the sucrose-free cocoa butter-based high-fat diet (C-HFD) feeding in mice leads to gut dysbiosis that associates with a pathologic phenotype marked by hepatic steatosis, low-grade inflammation, perturbed glucose homeostasis, and insulin resistance, compared with control mice fed the fish oil based high-fat diet (F-HFD). Results: C57BL/6 mice (5–6 mice/group) were fed two types of high fat diets (C-HFD and F-HFD) for 24 weeks. No significant difference was found in the liver weight or total body weight between the two groups. The 16S rRNA sequencing of gut bacterial samples displayed gut dysbiosis in C-HFD group, with differentially-altered microbial diversity or relative abundances. Bacteroidetes, Firmicutes, and Proteobacteria were highly abundant in C-HFD group, while the Verrucomicrobia, Saccharibacteria (TM7), Actinobacteria, and Tenericutes were more abundant in F-HFD group. Other taxa in C-HFD group included the Bacteroides, Odoribacter, Sutterella, Firmicutes bacterium (AF12), Anaeroplasma, Roseburia, and Parabacteroides distasonis. An increased Firmicutes/Bacteroidetes (F/B) ratio in C-HFD group, compared with F-HFD group, indicated the gut dysbiosis. These gut bacterial changes in C-HFD group had predicted associations with fatty liver disease and with lipogenic, inflammatory, glucose metabolic, and insulin signaling pathways. Consistent with its microbiome shift, the C-HFD group showed hepatic inflammation and steatosis, high fasting blood glucose, insulin resistance, increased hepatic de novo lipogenesis (Acetyl CoA carboxylases 1 (Acaca), Fatty acid synthase (Fasn), Stearoyl-CoA desaturase-1 (Scd1), Elongation of long-chain fatty acids family member 6 (Elovl6), Peroxisome proliferator-activated receptor-gamma (Pparg) and cholesterol synthesis (β-(hydroxy β-methylglutaryl-CoA reductase (Hmgcr). Non-significant differences were observed regarding fatty acid uptake (Cluster of differentiation 36 (CD36), Fatty acid binding protein-1 (Fabp1) and efflux (ATP-binding cassette G1 (Abcg1), Microsomal TG transfer protein (Mttp) in C-HFD group, compared with F-HFD group. The C-HFD group also displayed increased gene expression of inflammatory markers including Tumor necrosis factor alpha (Tnfa), C-C motif chemokine ligand 2 (Ccl2), and Interleukin-12 (Il12), as well as a tendency for liver fibrosis. Conclusion: These findings suggest that the sucrose-free C-HFD feeding in mice induces gut dysbiosis which associates with liver inflammation, steatosis, glucose intolerance and insulin resistance. Full article

Aphids are insect pests that suck phloem sap and introduce salivary proteins into plant tissues through saliva secretion. The effector of salivary proteins plays a key role in the modulation of host plant defense responses and enhancing aphid host adaptation. Based on previous transcriptome sequencing results, a candidate effector cyclin-dependent kinase-like (CDK) was identified from the grain aphid Sitobion avenae. In this study, the function of SaCDK in wheat defense response and the adaptation of S. avenae was investigated. Our results showed that the transient overexpression of SaCDK in tobacco Nicotiana benthamiana suppressed cell death triggered by mouse pro-apoptotic protein-BAX or Phytophthora infestans PAMP-INF1. SaCDK, delivered into wheat cells through a Pseudomonas fluorescens-mediated bacterial type III secretion system, suppressed callose deposition in wheat seedlings, and the overexpression of SaCDK in wheat significantly decreased the expression levels of salicylic acid and jasmonic acid signaling pathway-related genes phenylalanine ammonia lyase (PAL), pathogenesis-related 1 protein (PR1), lipoxygenase (LOX) and Ω-3 fatty acid desaturase (FAD). In addition, aphid bioassay results showed that the survival and fecundity of S. avenae were significantly increased while feeding on the wheat plants carrying SaCDK. Taken together, our findings demonstrate that the salivary protein SaCDK is involved in inhibiting host defense response and improving its host adaptation, which lays the foundation to uncover the mechanism of the interaction of cereal aphids and host plants. Full article

Angiopoietin-like 3 (ANGPTL3) is a hepatokine acting as a negative regulator of lipoprotein lipase (LPL). Vupanorsen, an ANGPTL3 directed antisense oligonucleotide, showed an unexpected increase in liver fat content in humans. Here, we investigated the molecular mechanism linking ANGPTL3 silencing to hepatocyte fat accumulation. Human hepatocarcinoma Huh7 cells were treated with small interfering RNA (siRNA) directed to ANGPTL3, human recombinant ANGPTL3 (recANGPTL3), or their combination. Using Western blot, Oil Red-O, biochemical assays, and ELISA, we analyzed the expression of genes and proteins involved in lipid metabolism. Oil Red-O staining demonstrated that lipid content increased after 48 h of ANGPTL3 silencing (5.89 ± 0.33 fold), incubation with recANGPTL3 (4.08 ± 0.35 fold), or their combination (8.56 ± 0.18 fold), compared to untreated cells. This effect was also confirmed in Huh7-LX2 spheroids. A total of 48 h of ANGPTL3 silencing induced the expression of genes involved in the de novo lipogenesis, such as fatty acid synthase, stearoyl-CoA desaturase, ATP citrate lyase, and Acetyl-Coenzyme A Carboxylase 1 together with the proprotein convertase subtilisin/kexin 9 (PCSK9). Time-course experiments revealed that 6 h post transfection with ANGPTL3-siRNA, the cholesterol esterification by Acyl-coenzyme A cholesterol acyltransferase (ACAT) was reduced, as well as total cholesterol content, while an opposite effect was observed at 48 h. Under the same experimental conditions, no differences in secreted apoB and PCSK9 were observed. Since PCSK9 was altered by the treatment, we tested a possible co-regulation between the two genes. The effect of ANGPTL3-siRNA on the expression of genes involved in the de novo lipogenesis was not counteracted by gene silencing of PCSK9. In conclusion, our in vitro study suggests that ANGPTL3 silencing determines lipid accumulation in Huh7 cells by inducing the de novo lipogenesis independently from PCSK9. Full article

Complement component 4 binding protein α (C4BPA) is an immune gene which is responsible for the complement regulation function of C4BP by binding and inactivating the Complement component C4b (C4b) component of the classical Complement 3 (C3) invertase pathway. Our previous findings revealed that C4BPA was differentially expressed by comparing the transcriptome in high-fat and low-fat bovine mammary epithelial cell lines (BMECs) from Chinese Holstein dairy cows. In this study, a C4BPA gene knockout BMECs line model was constructed via using a CRISPR/Cas9 system to investigate the function of C4BPA in lipid metabolism. The results showed that levels of triglyceride (TG) were increased, while levels of cholesterol (CHOL) and free fatty acid (FFA) were decreased (p < 0.05) after knocking out C4BPA in BMECs. Additionally, most kinds of fatty acids were found to be mainly enriched in the pathway of the biosynthesis of unsaturated fatty acids, linoleic acid metabolism, fatty acid biosynthesis, and regulation of lipolysis in adipocyte. Meanwhile, the RNA-seq showed that most of the differentially expressed genes (DEGs) are related to PI3K-Akt signaling pathway. The expressions of 3-Hydroxy-3-Methylglutaryl-CoA Synthase 1 (HMGCS1), Carnitine Palmitoyltransferase 1A (CPT1A), Fatty Acid Desaturase 1 (FADS1), and Stearoyl-Coenzyme A desaturase 1 (SCD1) significantly changed when the C4BPA gene was knocked out. Collectively, C4BPA gene, which is an immune gene, played an important role in lipid metabolism in BMECs. These findings provide a new avenue for animal breeders: this gene, with multiple functions, should be reasonably utilized. Full article

The aim of this study was to investigate the effects of dietary chitosan supplementation on the muscle composition, digestion, lipid metabolism, and stress resistance, and their related gene expression, of juvenile tilapia (Oreochromis niloticus) subjected to cadmium (Cd²⁺) stress. Juvenile tilapia with an initial body weight of 21.21 ± 0.24 g were fed with a formulated feed containing five different levels (0%, 0.5%, 1.0%, 1.5%, and 2.0%) of chitosan for 60 days, while the water in all experimental groups contained a Cd²⁺ concentration of 0.2 mg/L. The results showed that, compared with the control group (0% chitosan), the contents of crude fat and crude protein in the muscle, the activities of lipase, trypsin, and amylase in the intestine, as well as the relative expression levels of metallothionein (mt), cytochrome P450 1A (cyp1a), carnitine palmitoyltransferase-1 (cpt-1), peroxisome proliferator-activated receptor alpha (pparα), peroxisome proliferator-activated receptor gamma (pparγ), hormone-sensitive lipase (hsl), lipoprotein lipase (lpl), malate dehydrogenase (mdh), leptin (lep), fatty acid synthase (fas), sterol regulatory element-binding protein 1 (srebp1), and stearoyl-CoA desaturase (scd) genes in the liver of juveniles were significantly increased (p < 0.05). In conclusion, dietary chitosan supplementation could alleviate the effects of Cd²⁺ stress on the muscle composition, digestive enzymes, lipid metabolism, and stress resistance, and their related gene expression, of juvenile tilapia, and to some extent reduce the toxic effect of Cd²⁺ stress on tilapia. Full article