title: Hypolipidemic activity of okra is mediated through inhibition of lipogenesis and upregulation of cholesterol degradation.
abstract: Little is known about the hypolipidemic activity of okra; therefore, we investigated the hypolipidemic activity of okra and its interaction with gene expression of several key components involved in lipid homeostasis. Male C57BL/6 mice were randomly divided into three groups and fed with hyperlipidemic diet or two hyperlipidemic diets supplemented with 1% or 2% okra powder for eight weeks. Results demonstrated that okra dose-dependently decreased serum and hepatic total cholesterol and triglyceride, and enhanced fecal excretion of bile acids. Gene expression analysis revealed that okra upregulated cholesterol 7α-hydroxylase (CYP7A1) expression, downregulated expression of sterol regulatory element-binding protein 1c (SREBP1c) and fatty acid synthase (FAS), with no effect on sterol regulatory element-binding protein 2 (SREBP2), 3-hydroxy-3-methylglutaryl-CoA reductase (HMGR), low-density lipoprotein receptor (LDLR) and carnitine palmitoyltransferase-1A (CPT1A). It was suggested that hypolipidemic activity of okra was mediated most likely by upregulation of cholesterol degradation through CYP7A1 and by inhibition of lipogenesis through SREBP1c and FAS. Okra raw and fractionated polysaccharide showed strong bile acid binding capacity in vitro, which may contribute to the hypolipidemic activity observed. In conclusion, okra has potential application in the management of hyperlipidemia and its associated metabolic disorders.
authors.affiliation: College of Light Industry and Food Sciences, South China University of Technology, 381 Wushan Road, 510641, Guangzhou, China.
authors.forename: Hong
authors.initials: H
authors.lastname: Wang
authors.forename: Gu
authors.initials: G
authors.lastname: Chen
authors.forename: Dandan
authors.initials: D
authors.lastname: Ren
authors.forename: Shang-Tian
authors.initials: ST
authors.lastname: Yang
mesh_terms: D028483:Abelmoschus / Q000737:chemistry*; D050156:Adipogenesis / Q000235:genetics; D000818:Animals; D001647:Bile Acids and Salts / Q000378:metabolism; D002334:Carnitine O-Palmitoyltransferase / Q000235:genetics / Q000378:metabolism; D002784:Cholesterol / Q000097:blood; D002790:Cholesterol 7-alpha-Hydroxylase / Q000235:genetics / Q000378:metabolism*; D019587:Dietary Supplements; D064429:Fatty Acid Synthases / Q000235:genetics / Q000378:metabolism*; D006903:Hydroxymethylglutaryl CoA Reductases / Q000235:genetics / Q000378:metabolism; D006949:Hyperlipidemias / Q000188:drug therapy*; D050155:Lipogenesis / Q000187:drug effects*; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D011973:Receptors, LDL / Q000235:genetics / Q000378:metabolism; D051780:Sterol Regulatory Element Binding Protein 1 / Q000235:genetics / Q000378:metabolism*; D051782:Sterol Regulatory Element Binding Protein 2 / Q000235:genetics / Q000378:metabolism; D014280:Triglycerides / Q000097:blood; D015854:Up-Regulation
chemical_list: D001647:Bile Acids and Salts; D012333:RNA, Messenger; D011973:Receptors, LDL; C497388:Srebf1 protein, mouse; C497391:Srebf2 protein, mouse; D051780:Sterol Regulatory Element Binding Protein 1; D051782:Sterol Regulatory Element Binding Protein 2; D014280:Triglycerides; D002784:Cholesterol; D006903:Hydroxymethylglutaryl CoA Reductases; D002790:Cholesterol 7-alpha-Hydroxylase; C502772:Cyp7a1 protein, mouse; D002334:Carnitine O-Palmitoyltransferase; D064429:Fatty Acid Synthases
keywords: CYP7A1; FAS; SREBP1c; hypolipidemic activity; okra; polysaccharide