Background: miRNAs are single-stranded, small RNA molecules with a length of 18–25 nucleotides. They bind to the 3′ untranslated regions of mRNA transcripts to reduce the translation of these transcripts or to cause their degradation. The roles of these molecules differ in biological processes, such as cell differentiation, proliferation, apoptosis and tumor genesis. miRNA-33 is encoded by the gene introns of proteins that bind sterol-regulatory elements. This molecule cooperates with these proteins to control cholesterol homeostasis, fatty acid levels and the genes that are related to the expression of fat metabolism. The examination of miR-33 expression and its target genes can promote the in-depth study of the miRNA regulation mechanism in the formation process of goose fatty liver and can lay a foundation for research into human fatty liver. Methodology/principal findings: (1) Through real-time fluorescent quantitative polymerase chain reaction (TaqMan MicroRNA Assay), we detected the expression of miR-33 during the feeding of Landes geese. The expression level of miR-33 increases significantly in the liver after 19 days in comparison with the control group; (2) By using the bioinformatics software programs TargetScan, miRDB and miRCosm to predict the target genes of miR-33 according to laboratory prophase transcriptome results and references, we screen nine target genes: adenosine triphosphate binding cassette transporters A1, adenosine triphosphate binding cassette transporters G1, Neimann Pick C, carnitine O-octanoyltransferase (CROT), cyl-CoA dehydrogenase/3-ketoacyl-CoA thiolase/enoyl-CoA hydratase, beta subunit (HADHB), AMP-activated protein kinase, alpha subunit 1 (AMPKα1), insulin receptor substrate 2, glutamic pyruvate transaminase and adipose differentiation-related protein. The dual luciferase reporter gene system in the CHO cell line verifies that CROT, HADHB and NPC1 are the target genes of miR-33 in geese. The inhibition rate of CROT is highest and reaches 70%; (3) The seed sequence (5′ 2–8 bases) is the acting site of miR-33. The two predicted target sites of CROT are the target sites of miR-33. Moreover, the predicted target site of HADHB and NPC1 is the target site of miR-33. Conclusions/significance: (1) After 19 days of overfeeding, the expression level of miR-33 increases significantly in the livers of geese; (2) CROT, HADHB and NPC1 are the target genes of miR-33 in geese. These genes determine the combined target site.

Lead and cadmium are prevalent heavy metal toxins that contaminate the natural environment through animal husbandry and agricultural and industrial activities. Exposing dairy cows to these pollutants can have detrimental effects on milk production and quality, leading to health problems and decreasing the animals’ production performance. Therefore, investigating the distribution of lead and cadmium content and assessing the pollution levels at dairy farms are of significant theoretical and practical significance. This study determined the spatial distribution and clustering of lead and cadmium by sampling soil and feces from dairy farms in Jiangsu, China. The data obtained, in conjunction with soil data from Jiangsu Province, were used to evaluate the extent of lead and cadmium pollution at these farms. The results indicate that lead pollution levels are relatively low, whereas cadmium pollution is moderate in multiple regions. Ultimately, this study contributes to the assessment of the risks associated with lead and cadmium in dairy farming production and supports the establishment of a sustainable animal husbandry system, serving as an effective reference for subsequent ecological health farming, disease prevention, and management.

Inflammation often accompanies the development of liver diseases in humans, but appears to be repressed in geese. This study investigated the role of MAP3K7 C-terminal-like (MAP3K7CL) in goose fatty liver formation. Sixteen healthy 70-day-old male geese were randomly divided into control and overfed groups. Additionally, the transcriptome analysis after MAP3K7CL overexpression and lipopolysaccharide (LPS) treatment were performed in goose primary hepatocytes. The results showed that the MAP3K7CL mRNA expression was increased in the liver of overfed treatment compared to control group. Overexpression of MAP3K7CL in primary goose hepatocytes identified differentially expressed genes enriched in the mitogen-activated protein kinase (MAPK) signaling pathway. Specifically, DNA damage-inducible transcript 3 (DDIT3), insulin-like growth factor 1 receptor (IGF1R), neurofibromin 1 (NF1), and platelet-derived growth factor subunit B (PDGFB) were significantly downregulated upon MAP3K7CL overexpression, whereas heat shock protein family B member 1 (HSPB1) was significantly upregulated. Furthermore, transfection of goose hepatocytes with the MAP3K7CL overexpression vector lowered the expression of lipopolysaccharide-induced TNF factor (LITAF) and cysteinyl aspartate-specific proteinase-3, which are associated with inflammation and apoptosis, respectively. In accordance with these findings, DDIT3 and LITAF were downregulated in the overfed group, whereas HSPB1 was upregulated. Compared with the control, LPS treatment significantly decreased MAP3K7CL expression, while promoting that of LITAF and interleukin-6 (IL-6). Moreover, the combination of lipopolysaccharide and MAP3K7CL overexpression upregulated MAP3K7CL while downregulating LITAF and IL-6 with respect to LPS alone and empty vector control groups. Therefore, MAP3K7CL may inhibit the inflammatory response in goose fatty liver.