Background & Aims: Reversion-inducing cysteine-rich protein with Kazal motifs (RECK) is an extracellular matrix regulator with anti-fibrotic effects. However, its expression and role in metabolic dysfunction-associated steatohepatitis (MASH) and hepatic fibrosis are poorly understood.
Methods: We generated a novel transgenic mouse model with RECK overexpression specifically in hepatocytes to investigate its role in Western diet (WD)-induced liver disease.
Introduction Clinical nutrition for preterm and critically ill neonates remains a challenge. Preterms are often hemodynamically and metabolically compromised, which limits infusion volumes of nutrients and hinders achieving recommended nutrient intakes. While guidelines provide recommended ranges for parenteral nutrition (PN) intakes, they generally recommend enteral nutrition as soon as possible.
View Article and Find Full Text PDFNonalcoholic fatty liver disease (NAFLD) is characterized by excess lipid accumulation that can progress to inflammation (nonalcoholic steatohepatitis, NASH), and fibrosis. Serum β-hydroxybutyrate (β-HB), a product of the ketogenic pathway, is commonly used as a surrogate marker for hepatic fatty acid oxidation (FAO). However, it remains uncertain whether this relationship holds true in the context of NAFLD in humans.
View Article and Find Full Text PDFFor parenteral nutrition (PN) of newborns, the European Society for Paediatric Gastroenterology Hepatology and Nutrition (ESPGHAN) 2018 guidelines recommend standardized solutions over individual PN (IPN) solutions for most patients. This retrospective study assessed if a shift from IPN to standardized PN was feasible at the UZ Brussel. Using prescription data of 145 neonates, we calculated the nutrient provision for IPN and for standardized PN of the same volumes.
View Article and Find Full Text PDFRats selectively bred for the high intrinsic aerobic capacity runner (HCR) or low aerobic capacity runner (LCR) show pronounced differences in susceptibility for high-fat/high sucrose (HFHS) diet-induced hepatic steatosis and insulin resistance, replicating the protective effect of high aerobic capacity in humans. We have previously shown multiple systemic differences in energy and substrate metabolism that impacts steatosis between HCR and LCR rats. This study aimed to investigate hepatic-specific mechanisms of action via changes in gene transcription.
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