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Cell Metab
January 2025
Section of Endocrinology, Diabetes, and Metabolism, Department of Medicine, Baylor College of Medicine, Houston, TX, USA. Electronic address:
De novo lipogenesis (DNL) is the process whereby cells synthesize fatty acids from acetyl-CoA, contributing to steatosis in fatty liver disease. Two new studies, using genetic mouse models, metabolomics, and pharmacology, identified alternative pathways in DNL and unexpected physiological effects when targeting key enzymes in this pathway.
View Article and Find Full Text PDFSci Rep
January 2025
Iranian Research Institute of Plant Protection, Agricultural Research, Education and Extension Organization (AREEO), Tehran, Iran.
Winter wild oat (Avena sterilis subsp. ludoviciana (Durieu) Gillet & Magne) has been considered the most common and troublesome weed in wheat fields of Iran. The widespread and continuous use of herbicides has led to the emergence and development of resistant biotypes in A.
View Article and Find Full Text PDFNat Commun
January 2025
Department of Molecular Physiology of Exercise and Nutrition, German Institute of Human Nutrition (DIfE), Potsdam-Rehbruecke, Nuthetal, Germany.
Chem Biol Interact
December 2024
Department of Gastroenterology and Hepatology, Hangzhou Red Cross Hospital, Hangzhou, 310003, China. Electronic address:
Nonalcoholic Steatohepatitis (NASH) is a common liver disease with limited treatment options. Oxymatrine (OMT) has been reported to treat liver diseases effectively. This study aims to explore the mechanisms of OMT in NASH.
View Article and Find Full Text PDFAm J Pathol
December 2024
Division of Gastroenterology and Hepatology, Stanford University, Palo Alto, California; Palo Alto VA, Palo Alto, California. Electronic address:
Mitochondrial maladaptation and dysfunction contribute to the progression of metabolic dysfunction-associated steatohepatitis (MASH). The authors recently implicated the induction of Shc in progressive MASH during aging and the cytoplasmic p52Shc isoform in the activation of redox enzyme NOX2. The mitochondrial Shc isoform p46Shc was shown to repress acetyl-coenzyme A acyltransferase 2 (ACAA2) in vitro.
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