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Introduction: The therapeutic landscape of Metabolic dysfunction-Associated Steatotic Liver Disease (MASLD) is rapidly evolving with the FDA approval of resmetirom, the first authorized molecule to treat metabolic dysfunction-associated steatohepatitis. Clinical trials are investigating other promising molecules. However, this focus on pharmacotherapy may overshadow lifestyle interventions, which remain the cornerstone of MASLD management. A significant percentage of patients with MASLD struggle with an underlying eating disorder, often a precursor to obesity. The obesity pandemic, exacerbated by the increasing prevalence of binge eating, underscores the need for a psychological approach to address their common roots. Areas covered: We reviewed the current evidence on behavioral interventions for MASLD. Interventions such as self-monitoring, goal setting, and frequent counseling, have proven effective in achieving at least 5% weight loss. Cognitive behavioral therapy is the first-line treatment for eating disorders and has shown efficacy in treating binge eating and obesity. Further research is needed to establish the optimal behavioral therapy for MASLD, focusing on enhancing compliance and achieving sustained weight loss through diet and physical exercise. Expert opinion: The treatment of MASLD should not rely solely on pharmacotherapy targeting a single-organ manifestation. Instead, we must consider behavioral interventions, emphasizing the pivotal role of a holistic approach to this multifaceted disorder. [ABSTRACT FROM AUTHOR]

One flavonoid (quercetin, 1) and three dihydrochalcones (6''-O-p-hydroxybenzoyl-davidioside, 2, 4'-O-methyl-davidioside, 3, and davidioside, 4) were isolated from the leaves and young branches of Viburnum davidii Franch. All the structures were identified by comparison of their spectroscopic data (NMR and MS) with those present in literature. In addition, compounds 2–4 were evaluated for their cholinesterase inhibitory (ChEI) activity, for the first time. Accordingly, compounds 2 and 4 showed significant inhibition of both acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) with IC50 values equal to 36.883 and 39.274 µM, respectively for the former and 39.504 and 43.101 µM, respectively for the latter. [ABSTRACT FROM AUTHOR]

Abstract: Growing concern on the problem of mycotoxins in the alimentary chain underlines the need to investigate the mechanisms explaining the cholinergic effects of aflatoxin B1 (AFB1). We examined the effect of AFB1, a mycotoxin produced by Aspergillus flavus, on mouse brain acetylcholinesterase (AChE) and specifically on its molecular isoforms (G1 and G4) after in vitro exposure. AFB1 (from 10-9 to 10-4M), inhibited mouse brain AChE activity (IC50 = 31.6 × 10-6M) and its G1 and G4 molecular isoforms in a dose-dependent manner. Michaelis-Menten parameters indicate that the Km value increased from 55.2 to 232.2% whereas Vmax decreased by 46.2–75.1%. The direct, the Lineweaver-Burk and the secondary plots indicated a non-competitive-mixed type antagonism, induced when the inhibitor binds to the free enzyme and to the enzyme–substrate complex. AFB1-inhibited AChE was partially reactivated by pyridine 2-aldoxime (2-PAM) (10-4M) but the AChE-inhibiting time courses of AFB1 (10-4M) and diisopropylfluorophosphate (DFP) (2 × 10-7M) differed. Overall these data suggest that AFB1 non-competitively inhibits mouse brain AChE by blocking access of the substrate to the active site or by inducing a defective conformational change in the enzyme through non-covalent binding interacting with the AChE peripheral binding site, or through both mechanisms. [Copyright &y& Elsevier]