Download full-text PDF |
Source |
|---|
Publication Analysis
Top Keywords
Similar Publications
Methionine mitigates aflatoxicosis in quail chicks by improving gut microbiota, immunity, and meat quality.
Toxicol Rep
June 2025
Department of Animal Sciences, Faculty of Agriculture, University of Zabol, Sistan 98661-5538, Iran.
This study aimed to investigate the effects of dietary methionine (Met) supplementation on performance, immunity, and meat quality in growing Japanese quail exposed to aflatoxin B (AFB)-contaminated diets. Nine experimental diets were formulated, incorporating three levels of dietary Met (5.0, 6.
View Article and Find Full Text PDFCreatine monohydrate administration delayed muscle glycolysis of antemortem-stressed broilers by enhancing muscle energy status, increasing antioxidant capacity and regulating muscle metabolite profiles.
Poult Sci
January 2025
College of Animal Science and Technology, Qingdao Agricultural University, Qingdao 266000, China; Department of Biology and Agriculture, Zunyi Normal College, Ping`an Avenue, Hong Huagang District, Zunyi 563006, China.
Preslaughter stress induced a negative energy balance of broilers, resulted in an accelerated glycolysis and finally led to an inferior meat quality. The present study aimed to investigate the effects of creatine monohydrate (CMH) supplementation on muscle energy storage, antioxidant capacity, the glycolysis of postmortem muscle and the metabolite profiles in muscle of broilers subjected to preslaughter transport. Two hundred and forty broilers were chosen and randomly allocated into three treatments (group A, group B and group C), comprising 8 replicates (10 broilers each replicate).
View Article and Find Full Text PDFGenotype-Phenotype Correlations in the Hyperparathyroidism-Jaw Tumor Syndrome.
J Clin Endocrinol Metab
January 2025
Metabolic Diseases Branch, Bldg. 10/Rm 8C-101, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD 20892.
Establishing genotype-phenotype correlations in disorders of hereditary endocrine neoplasia is important for clinical screening, genetic counseling, prognostication, surveillance, and surgical strategy, and may also provide clues about disease pathogenesis. Important genotype-phenotype correlations are recognized, for example, in pheochromocytoma/paraganglioma and multiple endocrine neoplasia type 2A. The presence of such correlations has been less clear in other familial endocrine disorders associated with primary hyperparathyroidism including multiple endocrine neoplasia type 1 (MEN1), and the hyperparathyroidism-jaw tumor syndrome (HPT-JT).
View Article and Find Full Text PDFHomozygous MTAP deletion occurs in ~15% of cancers, making them vulnerable to decreases in the concentration of S-adenosylmethionine (SAM). AG-270/S095033 is an oral, potent, reversible inhibitor of methionine adenosyltransferase 2 A (MAT2A), the enzyme primarily responsible for the synthesis of SAM. We report results from the first-in-human, phase 1 trial of AG-270/S095033 as monotherapy in patients with advanced malignancies (ClinicalTrials.
View Article and Find Full Text PDFDeficiency of hepatokine orosomucoid1 aggravates NAFLD progression in mice.
Biochim Biophys Acta Mol Basis Dis
January 2025
Department of Clinical Pharmacy, School of Pharmacy, Naval Medical University/Second Military Medical University, Shanghai 200433, China. Electronic address:
Orosomucoid (ORM) is an important hepatokine that regulates metabolism. Previous report showed that isoform ORM2 but not ORM1 could downregulate lipogenic genes and ameliorate hepatic steatosis in obese mice, thereby categorizing ORM2 as a promising candidate for therapeutic intervention in nonalcoholic fatty liver disease (NAFLD). However, our previous studies found that mice lacking ORM1 gradually developed an obese phenotype with severe hepatic steatosis at the age of 24 weeks.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!