The fungicide propiconazole induces hepatic steatosis and activates PXR in a mouse model of diet-induced obesity.

Propiconazole is a triazole fungicide previously shown to induce triglyceride accumulation in human liver HepaRG cells, potentially via activation of the Pregnane X Receptor (PXR). However, whether propiconazole can disrupt hepatic and whole-body metabolism in vivo is currently unknown. Therefore, we aimed to examine the metabolic effects of propiconazole in the context of metabolic dysfunction-associated steatotic liver disease (MASLD), obesity, and insulin resistance.

The Lived Experience of Cardiac Arrest Survivors: A Scoping Review.

Background: Survival rates after cardiac arrest have steadily increased over the past few decades because of the adoption of cardiopulmonary resuscitation, public access to automated external defibrillators, and an increase in public education on how to perform cardiopulmonary resuscitation. The lived experiences of post-cardiac arrest survival have been underexplored. The themes that resulted from the analysis in this scoping review can inform clinical practice and propose strategies to improve the patients' quality of life.

Inhibition of activin receptor 2 signalling ameliorates metabolic dysfunction-associated steatotic liver disease in western diet/L-NAME induced cardiometabolic disease.

Objective: Blockade of activin 2 receptor (ACVR2) signaling has been shown to improve insulin sensitivity and aid in weight loss. Inhibition of ACVR2 signaling restores cardiac function in multiple heart failure models. However, its potential in the treatment of obesity-related cardiometabolic disease remains unknown.

Aortic Regurgitation: Review of Current Management.

Aortic regurgitation (AR) is a valvular disease characterized by retrograde blood flow from the aorta to the left ventricle. Various etiologies result in either an acute or chronic clinical presentation of AR and affect the severity of disease progression. Acute AR is a medical emergency caused by sudden increases in left ventricular volume.

Metabolic effects of nuclear receptor activation in vivo after 28-day oral exposure to three endocrine-disrupting chemicals.

Environmental exposure to endocrine-disrupting chemicals (EDCs) can lead to metabolic disruption, resulting in metabolic complications including adiposity, dyslipidemia, hepatic lipid accumulation, and glucose intolerance. Hepatic nuclear receptor activation is one of the mechanisms mediating metabolic effects of EDCs. Here, we investigated the potential to use a repeated dose 28-day oral toxicity test for identification of EDCs with metabolic endpoints.