Dietary carnosic acid suppresses hepatic steatosis formation via regulation of hepatic fatty acid metabolism in high-fat diet-fed mice.
- Author:
Mi Young PARK
1
;
Seong Taek MUN
Author Information
- Publication Type:Original Article
- Keywords: Carnosic acid; high-fat diet; hepatic steatosis; lipogenesis; fatty acid oxidation
- MeSH: Acyl Coenzyme A; Acyl-CoA Oxidase; Animals; Body Weight; Carnitine O-Palmitoyltransferase; Carrier Proteins; Diet; Diet, High-Fat; Diterpenes, Abietane; Fatty Acid Synthetase Complex; Fatty Acids, Monounsaturated; Glucose Tolerance Test; Hand; Homeostasis; Insulin Resistance; Lipogenesis; Liver; Mice; Oleic Acid; Palmitic Acid; Phenol; Plant Extracts; PPAR alpha; Stearoyl-CoA Desaturase
- From:Nutrition Research and Practice 2013;7(4):294-301
- CountryRepublic of Korea
- Language:English
- Abstract: In this study, we examined the hepatic anti-steatosis activity of carnosic acid (CA), a phenolic compound of rosemary (Rosmarinus officinalis) leaves, as well as its possible mechanism of action, in a high-fat diet (HFD)-fed mice model. Mice were fed a HFD, or a HFD supplemented with 0.01% (w/w) CA or 0.02% (w/w) CA, for a period of 12 weeks, after which changes in body weight, blood lipid profiles, and fatty acid mechanism markers were evaluated. The 0.02% (w/w) CA diet resulted in a marked decline in steatosis grade, as well as in homeostasis model assessment of insulin resistance (HOMA-IR) index values, intraperitoneal glucose tolerance test (IGTT) results, body weight gain, liver weight, and blood lipid levels (P < 0.05). The expression level of hepatic lipogenic genes, such as sterol regulating element binding protein-1c (SREBP-1c), liver-fatty acid binding protein (L-FABP), stearoyl-CoA desaturase 1 (SCD1), and fatty acid synthase (FAS), was significantly lower in mice fed 0.01% (w/w) CA and 0.02% (w/w) CA diets than that in the HFD group; on the other hand, the expression level of beta-oxidation-related genes, such as peroxisome proliferator-activated receptor alpha (PPAR-alpha), carnitine palmitoyltransferase 1 (CPT-1), and acyl-CoA oxidase (ACO), was higher in mice fed a 0.02% (w/w) CA diet, than that in the HFD group (P < 0.05). In addition, the hepatic content of palmitic acid (C16:0), palmitoleic acid (C16:1), and oleic acid (C18:1) was significantly lower in mice fed the 0.02% (w/w) CA diet than that in the HFD group (P < 0.05). These results suggest that orally administered CA suppressed HFD-induced hepatic steatosis and fatty liver-related metabolic disorders through decrease of de novo lipogenesis and fatty acid elongation and increase of fatty acid beta-oxidation in mice.
