The lipid from egg yolk is largely consumed in supplying the energy for embryonic growth until hatching. The remaining lipid in the yolk sac is transported into the hatchling’s tissues. The gene expression profiles of fast- and slow-growing chickens, Arbor Acres (AA) and Beijing-You (BJY), were determined to identify global differentially expressed genes and enriched pathways related to lipid metabolism in the pectoralis major at hatching. Between these two breeds, the absolute and weight-specific amounts of total yolk energy (TYE) and intramuscular fat (IMF) content in pectoralis major of fast-growing chickens were significantly higher (P < 0.01, P < 0.01, P < 0.05, respectively) than those of the slow-growing breed. IMF content and u-TYE were significantly related (r = 0.9047, P < 0.01). Microarray analysis revealed that gene transcripts related to lipogenesis, including PPARG, RBP7, LPL, FABP4, THRSP, ACACA, ACSS1, DGAT2, and GK, were significantly more abundant in breast muscle of fast-growing chickens than in slow-growing chickens. Conversely, the abundance of transcripts of genes involved in fatty acid degradation and glycometabolism, including ACAT1, ACOX2, ACOX3, CPT1A, CPT2, DAK, APOO, FUT9, GCNT1, and B4GALT3, was significantly lower in fast-growing chickens. The results further indicated that the PPAR signaling pathway was directly involved in fat deposition in pectoralis major, and other upstream pathways (Hedgehog, TGF-beta, and cytokine–cytokine receptor interaction signaling pathways) play roles in its regulation of the expression of related genes. Additional energy from the yolk sac is transported and deposited as IMF in the pectoralis major of chickens at hatching. Genes and pathways related to lipid metabolism (such as PPAR, Hedgehog, TGF-beta, and cytokine–cytokine receptor interaction signaling pathways) promote the deposition of IMF in the pectoralis major of fast-growing chickens compared with those that grow more slowly. These findings provide new insights into the molecular mechanisms underlying lipid metabolism and deposition in hatchling chickens.

Intramuscular fat (IMF)—an important factor affecting meat quality—can be appropriately increased by genetic selection. Chicken lines divergently selected for IMF content were used in this study to investigate the mechanisms behind differential IMF deposition. Sixty 15th generation chickens were genotyped using the IASCHICK 55K single nucleotide polymorphism (SNP) chip. After quality control, 59 chickens and 36,893 SNPs were available for subsequent analysis. Population structure assessment indicated that the lines were genetically differentiated. Based on the top 1% paired fixation index values, three pathways were significantly (p < 0.05) enriched, and nine genes were considered candidate genes for differential IMF deposition. Differences between the lines in the expressions of representative genes involved in the above pathways were detected in 16th generation chickens. This study suggests that genetic selection for increased IMF in the pectoralis major muscle may enhance fatty acid synthesis, transport, and esterification, and reduce triglyceride hydrolysis. The peroxisome proliferator-activated receptor (PPAR) signaling pathway, glycerolipid metabolism, and fatty acid degradation pathway may have contributed to the differences in IMF deposition between the lines. These results contribute to the understanding of the genetic mechanisms behind IMF deposition, and the improvement of chicken meat quality.

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.

Glucose metabolism plays an important role in many normal and pathological physiological processes in the body. The breakdown and synthesis of muscle glycogen provides ATP for muscle activities. A genome-wide association study for muscle glycogen was performed in 474 Jingxing yellow chickens to identify significant single nucleotide polymorphisms (SNPs) and insertions and deletions (INDELs) involved in muscle glycogen metabolism. A total of nine SNPs (p < 1/699341) and three INDELs (p < 1/755733) reached a significant level of potential association. The following results were obtained through a series of analyses, including additive effects and gene function annotation. Two significant SNPs were found in introns 12 and 13 of copine 4 (CPNE4) on chromosome 2. The wild-type and mutant individuals had significant differences in glycogen metabolism at two loci (p < 0.01 for both). Individuals carrying two mutations had increased muscle glycogen content. According to the gene annotation of chromosome 11, there is a significant INDEL in intron 6 of naked cuticle homolog 1 (NKD1). After the INDEL mutation, the glycogen content increased significantly. There was a significant difference between wild-type and mutant individuals (p < 0.01). These mutations likely affecting two genes (CPNE4 and NKD1) may affect glycogen storage in a pleiotropic manner. Gene annotation indicates that CPNE4 and NKD1 may affect the process of glucose metabolism. Our findings contribute to understanding the genetic regulation of muscle glycogen metabolism and provide theoretical support.

Abdominal fat percentage (AFP) is an important economic trait in chickens. Intensive growth selection has led to the over-deposition of abdominal fat in chickens, but the genetic basis of AFP is not yet clear. Using 520 female individuals from selection and control lines of Jingxing yellow chicken, we investigated the genetic basis of AFP using a genome-wide association study (GWAS) and fixation indices (F_ST). A 0.15 MB region associated with AFP was located on chromosome 27 and included nine significant single nucleotide polymorphisms (SNPs), which could account for 3.34–5.58% of the phenotypic variation. In addition, the π value, genotype frequency, and dual-luciferase results identified SNP rs312715211 in the intron region of ZNF652 as the key variant. The wild genotype was associated with lower AFP and abdominal fat weight (AFW), but higher body weight (BW). Finally, annotated genes based on the top 1% SNPs were used to investigate the physiological function of ZNF652. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis suggested that ZNF652 may reduce AFW and BW in broilers through the TGF-β1/SMad2/3 and MAPK/FoxO pathways via EGFR and TGFB1. Our findings elucidated the genetic basis of chicken AFP, rs312715211 on the ZNF652 gene, which can affect BW and AFW and was the key variant associated with AFP. These data provide new insight into the genetic mechanism underlying AF deposition in chickens and could be beneficial in breeding chickens for AF.