Genistein inhibits AOM/DSS-induced colon cancer by regulating lipid droplet accumulation and the SIRT1/FOXO3a pathway in high-fat diet-fed female mice. Issue 1 (1st January 2019)

• Record Type: Journal Article
• Authors: Qi, Wentao; Wang, Yong; Yao, Jinli; Sun, Hui; Duan, Xiaoliang; Song, Ge; Pang, Shaojie; Wang, Chunling; Li, Aike
• Is Part Of: Food and agricultural immunology. Volume 30:Issue 1(2019)
• Page Start: 1271
• Page End: 1285
• Publication Date: 2019-01-01
• Subjects: Genistein -- obesity -- lipid droplets -- colon cancer -- SIRT1/FOXO3a pathway; Immunochemistry -- Periodicals; Food -- Analysis -- Periodicals; Immunoassay -- Periodicals; 616.079
• DOI: 10.1080/09540105.2019.1684452
• Languages: English
• ISSNs: 0954-0105

Abstract

ABSTRACT: Obesity is one of the risk factors associated with colon cancer. In this study, we investigated the effect of genistein on colon cancer in obese mice and its underlying mechanism. Colon cancer was induced by azoxymethane/dextran sulfate sodium injection in Kun Ming mice, and they were fed with regular or high-fat diet (HFD). Genistein-rich diet (50, 150 and 450 mg/kg) decreased body weight gain, serum TC, TG, LDL-C levels, whereas it increased serum HDL-C level and lipase activity under HFD conditions. Genistein reduced mRNA levels of fat metabolism-related genes, including Fas and Acc1, and decreased levels of lipid droplet-related proteins, including perilipin, ADRP and TIP-47. Furthermore, genistein decreased PPAR-γ expression, whereas it increased SIRT1 and FOXO3 levels in colon tissue. Thus, genistein prevented the development of colon cancer by inhibiting abnormal fatty acid biosynthesis via regulation of the SIRT1/FOXO3a pathway in HFD-fed female mice.