CPT1A and metabolic dysfunction-associated steatotic liver disease: Du et al. reported that 15-week supplementation of β-glucan derived from L. edodes following 6-week NAFLD-induction by HFD not only could upregulate the hepatic expression of peroxisome proliferator-activated receptor α (PPARα) and carnitine palmitoyltransferase 1α (CPT1α) involved in fatty acid oxidation, but also inhibit the expression of cluster of differentiation 36 in the liver responsible for free fatty acid uptake [36,57].