Free fatty acids, 11β-hydroxysteroid dehydrogenase 1, Endoplasmic reticulum stress, CCAAT/enhancer-binding protein homologous protein, CCAAT/enhancer-binding protein α, Corticosterone, Nutritional diseases. Deficiency diseases, RC620-627

Abstract Objective Free fatty acids (FFA) can increase the expression of 11β-hydroxysteroid dehydrogenase 1 (11β-HSD1) in local tissues and organs. However, the mechanism underlying the effect of FFA on 11β-HSD1 expression remains unclear. Methods A total of 24 male Syrian golden hamsters (SPF grade) were selected and randomly divided into a control group (Con, n = 8) fed a normal diet, and a high-fat diet group (n = 16) fed for 12 weeks. After successfully establishing the hyperlipidemia hamster model, the high-fat group was further divided into a high-fat group (HF) and a fenofibrate intervention group (Feno). Following an oral fat tolerance test (OFTT), blood lipids and FFA levels were measured. The expression levels of endoplasmic reticulum stress (ERS) marker GRP78, downstream key molecule CHOP, C/EBPα, and 11β-HSD1 were analyzed using Western blot and RT-PCR. Results After OFTT, FFA levels in all three groups initially decreased and then increased, with the highest levels observed in the HF group (Ps 0.05). Hepatic FFA, 11β-HSD1, and corticosterone levels were highest in the HF group (Ps 0.05). Hepatic 11β-HSD1 and corticosterone levels were positively correlated with FFA levels (Ps