Project description:The unique fat storage and metabolic characteristics of goose liver is an important model for studying lipid metabolism in animals or humans. In this study, RNA sequencing technology was used to obtain the liver transcriptome of Sichuan white goose with significant weight difference in the same population, and differentially expressed genes and their pathways were identified, which may help to understand the mechanism of goose weight change. In addition, the identified candidate genes may be useful for molecular breeding of geese.
Project description:The experiment was conducted at the Kołuda Wielka Experimental Station of the National Research Institute of Animal Production (Kołuda Wielka, Poland). All birds were kept in semi-intensive rearing system according to the oat-fattening technology. At 15.5 weeks of age, 8 geese were selected and divided into two groups (n=4) depending on final body weight. Group I (light) were geese with the flock average weight of 7,10 kg, group II (heavy) consisted of geese with above-average growth potential, which achieved a body weight of 7,95 kg during the same time. Up to 20 min after slaughter, the whole pituitary and hypothalamus were collected and stabilized in RNAlater solution to RNA isolation purpose.
Project description:Geese have a high tolerance of massive energy intake and exhibit little pathological development. We assessed phenotypes and transcriptomes of Tianfu geese to investigate the dynamic expression network behind goose adipogenesis. Goose liver exhibited higher fat accumulation than adipose tissues during fattening. We identified differentially expressed genes that function in several important lipid metabolism pathways, immune response, regulation of cancer, and differentially expressed long noncoding RNAs that might be involved in regulation of these pathways. We found that genes like BGE1 and SCD, which have key roles in glycolysis and synthesis of fatty acids, had higher fold change in liver than in adipose tissue. we suppose that the evolutionary split from mammals in adipogenesis is a result of adaptive evolution to long-distance migration.
Project description:Lion-head goose is the only large goose species in China, and it was one of the largest goose species in the world. Our previous study firstly reported a chromosome-level genome assembly of Lion-head goose (Anser cygnoides), a native breed in South China, through the combination of PacBio, Bionano, and Hi-C technologies. The fat content of foie gras is augmented during its preparation due to the special feeding regimen. Lion-head geese have a strong tolerance of massive energy intake and show a priority of fat accumulation in liver tissue. In this study, we studied for the first time the important differential genes that regulate fatty liver in Lion-head goose. After high-intake feeding, the fatty livers of Lion-head geese were distinctly characterized. The revelation of gene regulation is an important basis for the study of liver development and molecular characteristics for the Lion-head goose. To analyze the excellent fatty liver performance of Lion-head goose at the molecular level, we performed whole transcriptome analysis by high-throughput RNA sequencing to analyze the key regulatory genes that determine the fatty livers in high-intake feeding group compared with the normal livers in normally-fed Lion-head geese. We identified 716 differentially expressed mRNAs, 145 differentially expressed circRNAs, and 39 differentially expressed lncRNAs in the fatty livers in high-intake feeding group compared with the normal livers in normally-fed Lion-head geese, including upregulated and downregulated genes, respectively. GO enrichment analysis showed that these genes were significantly enriched in molecular function, involved in extracellular regions, DNA-binding transcription factor activity, extracellular matrix, heme binding and other life activities. We chose differentially expressed genes involved in either upregulation or downregulation, and we additionally confirmed the accuracy of sequencing at the RNA level. In summary, our research suggested that these differentially expressed genes may play important roles in fatty liver development in Lion-head goose. However, the functions and mechanisms of these significantly differentially expressed genes should be investigated in future studies.
Project description:We identified the differentially expressed miRNAs in Landes goose liver after overfeeding for 21 days using high-throughput sequencing. We obtained 21453493 and 21525819 clean reads in normal liver and fatty liver by high-throughput sequencing, respectively. Of these clean reads, we respectively gained 9244896 and 9847086 miRNAs sequences in two groups by filtering the known non-miRNA reads, such as rRNA, tRNA, snRNA, and snoRNA by screening against ncRNA deposited in the GenBank and Rfam databases. These findings provided insights into the expression profiles of miRNAs in goose liver, and deepened our understanding of miRNAs in hepatic steatosis of geese.
Project description:Multiomics reveals persistence of obesity-associated immune cell phenotypes in adipose tissue during weight loss and subsequent weight regain
Project description:Most individuals do not maintain weight loss, and weight regain increases cardio-metabolic risk beyond that of obesity. Adipose inflammation directly contributes to insulin resistance; however, immune-related changes that occur with weight loss and weight regain are not well understood. Single cell RNA-sequencing was completed with CITE-sequencing and biological replicates to profile changes in murine immune subpopulations following obesity, weight loss, and weight cycling. Weight loss normalized glucose tolerance, however, type 2 immune cells did not repopulate adipose following weight loss. Many inflammatory populations persisted with weight loss and increased further following weight regain. Obesity drove T cell exhaustion and broad increases in antigen presentation, lipid handing, and inflammation that persisted with weight loss and weight cycling. This work provides critical groundwork for understanding the immunological causes of weight cycling-accelerated metabolic disease.
Project description:Background and aims: A coordinated stress and regenerative response is important following hepatocyte damage. Here, we investigate the phenotypes that result from genetic abrogation of individual components of the CHK2/ p53/ p21 pathway in a murine model of metabolic liver injury. Methods: NTBC was reduced or withdrawn in Fah / mice lacking Chk2, p53 or p21, and survival, tumor development, liver injury and regeneration were analyzed. Partial hepatectomies were performed and mice were challenged with the Fas-antibody Jo2. Results: In a model of metabolic liver injury, loss of p53, but not of Chk2, impairs the oxidative stress re-sponse and aggravates liver damage, indicative of a direct p53-dependent protective effect on hepatocytes. Cell cycle control during chronic liver injury critically depends on the presence of both p53 and its downstream effector p21. In p53-deficient hepatocytes, unchecked proliferation occurs despite a strong induction of p21, revealing a complex interdependency between p21 and p53. The increased regenerative potential in the absence of p53 cannot fully compensate the surplus injury and is not sufficient to promote survival. Despite the different phenotypes as-sociated with the loss of individual components of the DNA damage response, gene expression patterns are dominated by the severity of liver injury, but reflect distinct effects of p53 on prolif-eration and the anti-oxidative stress response. Conclusion: Characteristic phenotypes result from the genetic abrogation of individual components of the DNA damage response cascade in a liver injury model. The extent to which loss of gene function can be compensated, or affects injury and proliferation, depends on the level at which the cas-cade is interrupted.