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Fig. 5 | Molecular Medicine

Fig. 5

From: The protective effects of the β3 adrenergic receptor agonist BRL37344 against liver steatosis and inflammation in a rat model of high-fat diet-induced nonalcoholic fatty liver disease (NAFLD)

Fig. 5

β3-AR stimulation plays a role in alleviating liver steatosis associated with NAFLD. Treatment with the β3-AR agonist BRL37344 for 4 weeks decreased CD36 in NAFLD rats, thus decreasing FAs entry into hepatocytes. On the other hand, increases in mCPT-1 led to increased FAs entry into mitochondria. These two processes together caused a decrease in FA levels in hepatocytes. In addition, the increased FA levels in mitochondria and the increased PPAR-ɑ levels were beneficial for mitochondrial β-oxidation. BRL37344 also decreased PPAR-γ expression. All of the above factors contributed to the relief of liver steatosis in NAFLD rats. β3-AR: beta-3 adrenergic receptor; FAs: fatty acids; mCPT-1: mitochondrial carnitine palmitoyltransferase-1; PPAR-ɑ: peroxisome proliferator-activated receptor-alpha; PPAR-γ: peroxisome proliferator-activated receptor-gamma

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