The meat quality of chicken is an important factor affecting the consumer’s health. It was hypothesized that n-3 polyunsaturated fatty acid (n-3 PUFA) could be effectively deposited in chicken, by incorporating antioxidation of soybean isoflavone (SI), which led to improved quality of chicken meat for good health of human beings. Effects of partial or complete dietary substitution of lard (LA) with linseed oil (LO), with or without SI on growth performance, biochemical indicators, meat quality, fatty acid profiles, lipid-related health indicators and gene expression of breast muscle were examined in chickens. A total of 900 males were fed a corn–soybean meal diet supplemented with 4% LA, 2% LA + 2% LO and 4% LO and the latter two including 30 mg SI/kg (2% LA + 2% LO + SI and 4% LO + SI) from 29 to 66 days of age; each of the five dietary treatments included six replicates of 30 birds. Compared with the 4% LA diet, dietary 4% LO significantly increased the feed efficiency and had no negative effect on objective indices related to meat quality; LO significantly decreased plasma triglycerides and total cholesterol (TCH); abdominal fat percentage was significantly decreased in birds fed the 4% LO and 4% LO + SI diets. Chickens with LO diets resulted in higher contents of α-linolenic acid (C18:3n-3), EPA (C20:5n-3) and total n-3 PUFA, together with a lower content of palmitic acid (C16:0), lignoceric acid (C24:0), saturated fatty acids and n-6:n-3 ratio in breast muscle compared to 4% LA diet (P < 0.05); they also significantly decreased atherogenic index, thrombogenic index and increased the hypocholesterolemic to hypercholesterolemic ratio. Adding SI to the LO diets enhanced the contents of EPA and DHA (C22:6n-3), plasma total superoxide dismutase, reduced glutathione (GSH)/oxidized glutathione and muscle GSH content, while decreased plasma total triglyceride and TCH and malondialdehyde content in plasma and breast muscle compared to its absence (P < 0.05). Expression in breast muscle of fatty acid desaturase 1 ( FADS1), FADS2, elongase 2 ( ELOVL2) and ELOVL5 genes were significantly higher with the LO diets including SI than with the 4% LA diet. Significant interactions existed between LO level and inclusion of SI on EPA and TCH contents. These findings indicate that diet supplemented with LO combined with SI is an effective alternative when optimizing the nutritional value of chicken meat for human consumers.

Excessive deposition of abdominal fat is a public concern in the yellow chicken industry related to human nutrition. The common practice of nutritionists is to increase the fiber content in feed to control abdominal fat deposition of chickens. Corncob meal (CCM) is the cheapest ingredient widely used in animal diets. The possible effects of CCM on chicken abdominal fat deposition and the possible mechanism involving cecal microbiota remain unknown. The objectives of this study were to investigate the effects of CCM in modulating abdominal fat deposition and the role of the cecal microbiota and their metabolites. A total of 200 ninety-day-old Huxu female chickens were divided into 2 dietary treatments, each with 10 replicates of 10 birds, and were fed two finisher diets, from 90 to 135 d. The diets were a typical corn-soybean control diet (CON) and that diet with CCM partially replacing corn and corn gluten meal. Results showed that the CCM diet markedly decreased live weight and abdominal fat percentage (P < 0.05); chickens fed the CCM diet exhibited lower (P < 0.01) expression in abdominal fat of fatty acid binding protein 4 ( FABP4 ), stearoyl-CoA desaturase ( SCD ), fatty acid synthase ( FAS ), and peroxisome proliferator-activated receptor γ ( PPARγ ) but higher (P < 0.05) expression of estrogen receptor alpha ( ESR1 ). The CCM increased the abundance of Akkermansia (P < 0.05) and markedly reduced the relative cecal abundance of Phascolarctobacterium (P < 0.01), Rikenellaceae (P < 0.05), and Faecalibacterium (P < 0.01). The metabolomic and biochemical analyses demonstrated that the CCM diet increased (P < 0.05) the concentrations of butyrate in cecal contents. The majority of the metabolites in cecal digesta with differences in abundance were organic acids. The CCM diet increased (P < 0.05) contents of (R)-5-diphosphomevalote, pantothenic acid, 2-epi-5-epi-valiolone 7-phosphate, D-ribose 5-diphosphate, arbutin 6-phosphate, D-ribitol 5-phosphate, undecanoic acid, nicotinic acid, 4-methyl-2-oxovaleric acid, while decreasing (P < 0.05) those of oleic acid, glutaric acid, adipic acid, suberic acid, and L-fuculose 1-phosphate. In conclusion, these findings demonstrated that the dietary CCM treatment significantly decreased abdominal fat and altered the cecal microbiota and metabolite profiles of the yellow chickens.

Improving feed efficiency is a major goal in poultry production to reduce production costs and increase profitability. The genomic variants and possible molecular mechanisms responsible for residual feed intake (RFI) in chickens, however, remain poorly understood. In this study, using both local and commercial breeds, genome re-sequencing of low RFI and high RFI chickens was performed to elucidate the genomic variants underlying RFI. Results showed that 8,505,214 and 8,479,041 single nucleotide polymorphisms (SNPs) were detected in low and high RFI Beijing-You chickens, respectively; 8,352,008 and 8,372,769 SNPs were detected in low- and high-RFI Cobb chickens, respectively. Through a series of filtering processes, 3746 candidate SNPs assigned to 1137 genes in Beijing-You chickens and 575 candidate SNPs (448 genes) in Cobb chickens were found. The validation of the selected 191 SNPs showed that 46 SNPs were significantly associated with the RFI in an independent population of 779 Cobb chickens, suggesting that the method of screening associated SNPs with whole genome sequencing (WGS) strategy was reasonable. Functions annotation of RFI-related genes indicated that genes in Beijing-You were enriched in lipid and carbohydrate metabolism, as well as the phosphatase and tensin homolog (PTEN) signaling pathway. In Cobb, however, RFI-related genes were enriched in the feed behavior process and cAMP responsive element binding protein (CREB) signaling pathway. For both breeds, organismal development physiological processes were enriched. Correspondingly, NOS1, PHKG1, NEU3 and PIP5K1B were differentially expressed in Beijing-You, while CDC42, CSK, PIK3R3, CAMK4 and PLCB4 were differentially expressed in Cobb, suggesting that these might be key genes that contribute to RFI. The results of the present study identified numerous novel SNPs for RFI, which provide candidate biomarkers for use in the genetic selection for RFI. The study has improved knowledge of the genomic variants and potential biological pathways underlying RFI in chickens.

Caponization results in reduced androgen levels, which leads to abdominal fat accumulation in capons. In this study, we sought to understand the molecular mechanisms behind this fat accumulation. Abdominal fat (AF) content increased significantly (P < 0.05) and serum and AF testosterone levels decreased significantly (P < 0.05 or P < 0.01) after caponization. In AF tissue, 90 differentially expressed genes related to lipid metabolism were screened by gene expression profiling in caponized and sham-treated chickens. Among these, six representative genes were significantly up-regulated (APOA1, SCD, FABP7, RXRG, and FADS2) or down-regulated (FABP3) (P < 0.05 or P < 0.01) and were strongly associated with the PPAR pathway. In addition, cell junction pathways were also enriched. In vitro, Fat content was significantly lower in cells treated with testosterone compared with control cells (P < 0.01), and mRNA levels of RXRG, FABP7, and FABP3 changed accordingly, confirming the effect of testosterone on fat deposition. The results of this study indicate that testosterone reduction likely regulates gene expression through PPAR and cell junction pathways resulting in increased fat accumulation. These results provide increase our understanding of the biological mechanisms by which caponization induces greater fat accumulation.

The gut microbiota critically regulates lipid metabolism through microbial metabolites and host signaling pathways. Short-chain fatty acids (SCFAs), derived from dietary fiber fermentation, suppress hepatic lipogenesis via inhibition of SREBP-1c and enhance mitochondrial β-oxidation through GPR41/43 activation. Microbial enzymes convert primary bile acids into secondary bile acids, which activate FXR to inhibit lipogenesis and TGR5 to promote adipose thermogenesis. Lipopolysaccharide (LPS) from dysbiotic microbiota triggers TLR4-NF-κB signaling, exacerbating insulin resistance and adipose inflammation. Branched-chain amino acids (BCAAs), metabolized by gut microbes, drive adipogenesis via mTORC1-PPARγ signaling, with elevated circulating BCAAs linked to obesity. In livestock, microbiota modulation optimizes fat deposition: probiotics in pigs enhance intramuscular fat via Lactobacillus-enriched communities, while dietary succinate or coated sodium propionate reduces abdominal fat in broilers by reshaping cecal microbiota. Fecal microbiota transplantation confirms microbial causality in transferring fat phenotypes. Dysbiosis-associated mechanisms are conserved across species, where SCFAs and bile acids ameliorate metabolic inflammation, whereas LPS and BCAA imbalances worsen lipid dysregulation. Metabolic disorders, including obesity, type 2 diabetes (T2D), and non-alcoholic fatty liver disease (NAFLD), are tightly linked to gut microbiota perturbations. Dysbiosis drives LPS translocation and barrier impairment. These changes, along with altered metabolites, promote inflammation and fat deposition. Future strategies should integrate multi-omics and precision engineering of microbial consortia to advance therapies for both livestock and human metabolic health.

Salmonella typhimurium (ST) is a common foodborne pathogen that severely affects the health of humans and livestock. Protocatechuic acid (PCA) has been shown to possess anti-inflammatory and anti-bacterial functions. Chickens were used to investigate the effect of PCA on the gut health infected with ST. A total of one hundred eighty, 1-d-old birds were randomly allocated into 3 treatments, each with 6 replicates per treatment and 10 chicks per replicate. Broiler chicks in the control and ST treatment were fed a basal diet, and birds in the PCA+ST treatment received the basal diet with 600 mg/kg PCA. On d 14 and 16 of the trial, broilers in ST and PCA+ST treatments received an oral dose of ST, while broilers in CON received an equal amount of PBS. The data were analyzed by the one-way ANOVA. Dietary PCA increased (P < 0.05) final body weight, average daily gain, and feed to gain ratio in ST-challenged Yellow broilers. Protocatechuic acid significantly alleviated ST-induced intestinal mucosal injury reflected in the decreased (P < 0.05) plasma activity of diamine oxidase and ileal apoptosis, with increased (P < 0.05) ileal villus height and villus height/crypt depth. Protocatechuic acid treatment significantly decreased (P < 0.05) ST-induced proinflammatory cytokine (Interleukin-1β, Interleukin-6, Tumor necrosis factor-α, and Interferon-β) content in ileum. Meanwhile, PCA treatment significantly increased (P < 0.05) the transcript abundances of claudin 1 ( CLDN1 ), zonula occludens-1 ( ZO-1 ), and mucin 2 ( MUC2 ) in ileum, all related to the intestinal barrier in ST-challenged Yellow broilers. Additionally, PCA also increased (P < 0.05) the diversity and richness of the cecal microflora as reflected by reduced (P < 0.05) abundance of Bacteroidota, Proteobacteria and Escherichia-Shigella, and increased (P < 0.05) abundance of Firmicutes and Lactobacillus in ST-challenged Yellow broilers. These findings indicate that PCA relieves ST-induced loss weight, intestinal barrier injury, inflammatory response, and improves intestinal microbiota composition in Yellow broilers.