Objective To study the effects of antibiotics and high-fat diet on energy metabolism and the browning of white adipose tissue (WAT) and brown adipose tissue (BAT) in mice, so as to provide new ideas for the possible mechanism of adipose tissue in the prevention and treatment of obesity. Methods A total of 80 10-week-old C57BL/6 male mice were fed with normal diet in the early stage, and the antibiotic gavage group (AG) and antibiotic high-fat group (AFG) were given mixed antibiotics by gavage. The blank group (BG) and the high-fat diet group (FG) were given normal saline intragastric solution for 2 weeks, and after the gavage operation, the FG group and the AFG group were given high-fat diet for obesity modeling, and the BG group and AG group continued to be fed with normal diet for 8 weeks (N=20). After the experiment, each group was injected with β3-adrenergic receptor agonists for 5 days, and the high-fat/ordinary diet remained unchanged. At the end of the experiment, basal metabolic rate (BMR), fasting blood glucose (FBG) and rectal temperature were measured, and feces, blood, subcutaneous white fat, epididymis and brown adipose tissue in the scapular area of mice were collected. The automatic biochemical analyzer was used to determine the blood biochemical indexes; reverse transcription polymerase chain reaction (RT-qPCR) was used to measure the expression of genes related to browning of WAT and BAT adipose tissue, respectively. Real-time quantitative polymerase chain reaction (qPCR) was used to determine the expression of WAT mitochondrial DNA (mt DNA). Results From the 4th week to the end of the experiment, the weight of the AFG group was significantly higher than that of the AG group and significantly lower than that of the FG group (P<0.05). The body weight, organ coefficient, serum TC level, rectal temperature and WAT cell diameter in the AFG group were significantly higher than those in the AG group. The serum levels of FBG, TC and LDL in the AFG group were significantly lower than those in the FG group (P<0.05). The overall BMR(mlO2/h) FG group was significantly higher than that of BG group, and the AFG group was significantly higher than that of AG. BMR per unit body weight (mlO2/h/g) AFG was significantly higher than that of FG group (P<0.05). The expressions of RIP140, PPAR-γ and UCP-1 in BAT in the AFG group were significantly higher than those in the FG group, and the mt DNA copy number of WAT in the AFG group was significantly higher than that in the FG group (P<0.05). Conclusion Antibiotic intervention can up-regulate the expression of brown fat-related genes in high-fat diet mice, increase brown fat activity, increase the relative mitochondrial number of white fat, increase the level of browning of white fat, promote thermogenesis, increase the BMR per unit body weight of adult obese mice, and then improve the overall energy metabolism of the body, and slow down the weight gain induced by high-fat diet to a certain extent.

Objective To screen the key Mutation Genes in endometrial adenocarcinoma and study the relationship between their expression and immune response and prognosis. Methods The data of 543 cases of endometrial adenocarcinoma and 177 cases of normal tissues were downloaded from the Cancer Genome Atlas (TCGA) and genotype tissue expression (GTEX) for bioinformatics analysis. 22 cases of endometrial adenocarcinoma were collected, RT-qPCR was used to verify the gene expression. Results More than 96.38% of the patients had mutations, including missense mutation, single nucleotide mutation and C>T mutation. The top 10 mutations were PTEN, PIK3CA, TTN, ARID1A, TP53, MUC16, PIK3R1, KMT2D, CTCF and CSMD3. In TCGA, the expression of TP53 mutant was significantly higher than that of wild type (P<0.0001). The expression of TP53 in cancer tissue was higher than that in normal tissue, and the expression of TP53 mutant was higher than that of wild type (P<0.05). The overall survival (OS), progression free survival (PFS), disease free survival (DFS) and disease free survival (DSS) of TP53 mutant were lower than those of TP53 wild type (P<0.0001, P<0.0001, P=0.001, P<0.0001). A total of 344 differentially expressed genes (195 up-regulated and 149 down regulated) were identified in wild-type and mutant TP53. Compared with the wild type, the mutant was negatively enriched in the ^“immune effector process^”, ^“immune response^”, ^“immune system progress^”, ^“innate immune response^” and ^“immune response regulation^” pathways (P=0.001). The scores of T cell CD8 +, neutrophil, macrophages and meyloid dendritic cells of TP53 mutant were lower than those of wild type. Conclusion TP53 is highly expressed in endometrioid adenocarcinoma, and the expression of mutant is higher than that of wild type. TP53 mutation is positively correlated with poor prognosis and can inhibit immune response.