Download full-text PDF

Source

Publication Analysis

Top Keywords

acetyl coenzyme
4
coenzyme carboxylase
4
carboxylase effects
4
effects biotin
4
biotin deficiency
4
deficiency enzyme
4
enzyme rat
4
rat liver
4
liver adipose
4
adipose tissue
4

Similar Publications

Advancing de novo lipogenesis: Genetic and metabolic insights.

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 PDF

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 PDF

Pantothenate kinase 4 controls skeletal muscle substrate metabolism.

Nat Commun

January 2025

Department of Molecular Physiology of Exercise and Nutrition, German Institute of Human Nutrition (DIfE), Potsdam-Rehbruecke, Nuthetal, Germany.

Article Synopsis
  • Metabolic flexibility in skeletal muscle is crucial for healthy glucose and lipid metabolism, and its dysfunction can lead to metabolic diseases.
  • Exercise improves metabolic flexibility and helps identify mechanisms that support metabolic health.
  • The study reveals that pantothenate kinase 4 (PanK4) is vital for muscle metabolism, as its deletion disrupts fatty acid oxidation and elevates harmful acetyl-CoA levels, which lead to glucose intolerance, while increasing PanK4 enhances glucose uptake and lowers acetyl-CoA.
View Article and Find Full Text PDF

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 PDF

P46Shc Inhibits Mitochondrial ACAA2 Thiolase, Exacerbating Mitochondrial Injury and Inflammation in Aging Livers.

Am 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.

View Article and Find Full Text PDF

Want 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!