Thiram, a commonly used agricultural insecticide and fungicide, has been found to cause tibial dyschondroplasia (TD) in broilers, leading to substantial economic losses in the poultry industry. In this study, we aimed to investigate the mechanism of action of leucine in mitigating thiram-induced TD and leucine effects on gut microbial diversity. Broiler chickens were randomly divided into five equal groups: control group (standard diet), thiram-induced group (thiram 80 mg/kg from day 3 to day 7), and different concentrations of leucine groups (0.3%, 0.6%, 0.9% leucine from day 8 to day 18). Performance indicator analysis and tibial parameter analysis showed that leucine positively affected thiram-induced TD broilers. Additionally, mRNA expressions and protein levels of HIF-1α/VEGFA and Ihh/PTHrP genes were determined via quantitative real-time polymerase chain reaction and western blot. The results showed that leucine recovered lameness disorder by downregulating the expression of HIF-1α, VEGFA, and PTHrP while upregulating the expression of Ihh. Moreover, the 16 S rRNA sequencing revealed that the leucine group demonstrated a decrease in the abundance of harmful bacteria compared to the TD group, with an enrichment of beneficial bacteria responsible for producing short-chain fatty acids, including Alistipes, Paludicola, CHKCI002, Lactobacillus, and Erysipelatoclostridium. In summary, the current study suggests that leucine could improve the symptoms of thiram-induced TD and maintain gut microbiota homeostasis.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/j.ecoenv.2024.116260 | DOI Listing |
Proc Natl Acad Sci U S A
January 2025
Department of Entomology, University of California, Riverside, CA 92521.
Female mosquitoes require a vertebrate blood meal to activate reproduction, transmitting numerous devastating human diseases. Vitellogenesis is a central event of female reproduction that involves the massive production of vitellogenin (Vg) in the fat body and the maturation of ovaries. This process is controlled by the steroid hormone 20-hydroxyecdysone (20E); however, its molecular regulatory basis remains not completely understood.
View Article and Find Full Text PDFHLA
January 2025
Immunology Unit, Clinical Analysis Department, Albacete University Hospital Complex, Albacete, Spain.
HLA-DRB1*08:130 shows a Leucine at position 64 not described previously.
View Article and Find Full Text PDFVet Res Commun
January 2025
Laboratory of Veterinary Physiology, Department of Veterinary Medicine, Faculty of Agriculture, Tokyo University of Agriculture and Technology, 3-5-8 Saiwai-Cho, 183-8509, Fuchu, Tokyo, Japan.
This study investigated, for the first time, the alterations in the uterine echotexture and blood flow in cyclic and acyclic (inactive ovary) goats using ultrasonography. The study aimed also to evaluate the metabolomic changes in the plasma of cyclic and acyclic goats. Furthermore, the histopathological approach was applied to the specimens of the uterus to validate the findings of this study.
View Article and Find Full Text PDFMol Metab
January 2025
Arthur Riggs Diabetes and Metabolism Research Institute, City of Hope, Duarte, CA 91010, USA; Department of Translational Research and Cellular Therapeutics, City of Hope, Duarte, CA 91010, USA. Electronic address:
Objective: Loss of functional β-cell mass is a major cause of diabetes. Thus, identifying regulators of β-cell health is crucial for treating this disease. The In this study, we assessed the regulation of Lgr4 in islets, and the role of LGR4 and LGR4/RANK stoichiometry in β-cell health under basal and stress-induced conditions, in vitro and in vivo.
View Article and Find Full Text PDFMol Genet Metab
December 2024
Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX, USA; Texas Children's Hospital, Houston, TX, USA; BCM-CUHK Center of Medical Genetics, Prince of Wales Hospital, Hong Kong, China.
The 3-methylglutaconic aciduria (3-MGA-uria) syndromes comprise a heterogeneous group of inborn errors of metabolism defined biochemically by detectable elevation of 3-methylglutaconic acid (3-MGA) in the urine. In type 1 (or primary) 3-MGA-uria, distal defects in the leucine catabolism pathway directly cause this elevation. Secondary 3-MGA-uria syndromes, however, are unrelated to leucine metabolism-specific defects but share a common biochemical phenotype of elevated 3-MGA.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!