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Attenuating hyperammonemia preserves protein synthesis and muscle mass via restoration of perturbed metabolic pathways in bile duct-ligated rats.
Metab Brain Dis
January 2025
Hepato-Neuro Laboratory, Centre Hospitalier de l'Université de Montréal (CRCHUM), Université de Montréal, 900, Rue Saint-Denis - Pavillon R, R08.422, Montréal (Québec), H2X 0A9, Canada.
Sarcopenia and hepatic encephalopathy (HE) are complications of chronic liver disease (CLD), which negatively impact clinical outcomes. Hyperammonemia is considered to be the central component in the pathogenesis of HE, however ammonia's toxic effects have also been shown to impinge on extracerebral organs including the muscle. Our aim was to investigate the effect of attenuating hyperammonemia with ornithine phenylacetate (OP) on muscle mass loss and associated molecular mechanisms in rats with CLD.
View Article and Find Full Text PDFBackground & Aims: Hepatic insulin resistance is a fundamental phenomenon observed in both Type 2 diabetes (T2D) and metabolic (dysfunction) associated fatty liver disease (MAFLD). The relative contributions of nutrients, hyperinsulinemia, hormones, inflammation, and other cues are difficult to parse as they are convoluted by interplay between the local and systemic events. Here, we used a well-established human liver microphysiological system (MPS) to establish a physiologically-relevant insulin-responsive metabolic baseline and probe how primary human hepatocytes respond to controlled perturbations in insulin, glucose, and free fatty acids (FFAs).
View Article and Find Full Text PDFHawthorn carbon dots: a novel therapeutic agent for modulating body weight and hepatic lipid profiles in high-fat diet-fed mice.
Nanoscale
January 2025
Tang Center of Herbal Medicine Research and Department of Anesthesia & Critical Care, University of Chicago, Chicago, IL, 60637, USA.
Obesity, a chronic metabolic disorder characterized by excessive body weight and adipose tissue accumulation, is intricately linked to a spectrum of health complications. It is driven by a confluence of factors, including gut microbiota dysbiosis, inflammation, and oxidative stress, which are pivotal in its pathogenesis. A multifaceted therapeutic strategy that targets these interrelated pathways is essential for effective obesity management.
View Article and Find Full Text PDFCellular interactions in self-directed immune mediated liver diseases.
J Hepatol
January 2025
Centre for Liver and Gastroenterology research, Institute of Immunology and Immunotherapy, University of Birmingham, Birmingham, UK; National Institute of Health Research Biomedical Research Centre, University of Birmingham and University Hospital Birmingham NHS Foundation Trust, Birmingham, UK; Centre for Rare Diseases, European Reference Network on Hepatological Diseases (ERN-RARE-LIVER) centre, University of Birmingham, Birmingham, UK; Liver Transplant and Hepatobiliary department, Queen Elizabeth Hospital, University Hospital Birmingham NHS Foundation Trust, Birmingham, UK. Electronic address:
The lymphocyte population must traverse a complex path throughout their journey to the liver. The signals which these cells must detect, including cytokines, chemokines and other soluble factors, steer their course towards further crosstalk with other hepatic immune cells, hepatocytes and biliary epithelial cells. A series of specific chemokine receptors and adhesion molecules drive not only the recruitment, migration, and retention of these cells within the liver, but also their localisation.
View Article and Find Full Text PDFMulti-miRNAs-Mediated Hepatic Lepr Axis Suppression: A Pparg-Dicer1 Pathway-Driven Mechanism in Spermatogenesis for the Intergenerational Transmission of Paternal Metabolic Syndrome.
Adv Sci (Weinh)
January 2025
Fujian Key Laboratory of Coastal Pollution Prevention and Control, Xiamen University, Xiamen, 361102, China.
Bisphenol A (BPA) is an "environmental obesogen" and this study aims to investigate the intergenerational impacts of BPA-induced metabolic syndrome (MetS), specifically focusing on unraveling mechanisms. Exposure to BPA induces metabolic disorders in the paternal mice, which are then transmitted to offspring, leading to late-onset MetS. Mechanistically, BPA upregulates Srebf1, which in turn promotes the Pparg-dependent transcription of Dicer1 in spermatocytes, increasing the levels of multiple sperm microRNAs (miRNAs).
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