Key Laboratory of Endocrinology of National Health Commission, Department of Endocrinology, Peking Union Medical College Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing, China.
Department of Pharmacology, China-Beijing Institute of Heart, Lung and Blood Vessel Disease, Beijing Anzhen Hospital, Capital Medical University, Beijing, China.
J Diabetes Investig. 2020 Nov;11(6):1457-1469. doi: 10.1111/jdi.13285. Epub 2020 Jun 5.
AIMS/INTRODUCTION: Safflower yellow (SY) and its main component, hydroxysafflor yellow A, have been demonstrated to show anti-obesity effects. Peroxisome proliferator-activated receptor-γ2 (PPARγ2) is a critical transcription factor in adipose tissue metabolism. The aim of the present study was to explore the effects of SY in high-fat diet-induced obese mice, and further investigate the mechanism involving PPARγ2.
High-fat diet-induced obese mice were given 120 mg/kg/day SY for 8 weeks. Glucose and insulin tolerance tests were carried out. Fat mass and serum levels of glucose and insulin were measured. The expression of insulin signaling pathway-related genes and PPARγ2 in the adipose tissue was measured. In vitro, the effects of SY (0-500 mg/L) and hydroxysafflor yellow A (0-100 mg/L) on PPARγ2 promoter activities and PPARγ2 messenger ribonucleic acid (mRNA) levels in 3T3-L1 preadipocytes or adipocytes were also detected.
Safflower yellow reduced fat mass, decreased glucose levels and improved insulin sensitivity in obese mice. SY also increased the mRNA levels of insulin signaling pathway-related genes, and increased PPARγ2 mRNA levels by 39.1% in subcutaneous adipose tissue (P < 0.05). In vitro, SY and hydroxysafflor yellow A significantly enhanced PPARγ2 promoter activities by 1.3-2.1-fold, and increased PPARγ2 mRNA levels by 1.2-1.6-fold in 3T3-L1 preadipocytes or adipocytes (P < 0.05).
SY could reduce fat mass, decrease glucose levels and improve insulin sensitivity in high-fat diet-induced obese mice. The probable mechanism is to increase PPARγ2 expression by stimulating PPARγ2 promoter activities, further increasing the expression of insulin signaling pathway-related genes in subcutaneous adipose tissue.
目的/引言：红花黄色素（SY）及其主要成分羟基红花黄色 A 已被证明具有抗肥胖作用。过氧化物酶体增殖物激活受体-γ2（PPARγ2）是脂肪组织代谢中关键的转录因子。本研究旨在探讨 SY 对高脂饮食诱导肥胖小鼠的作用，并进一步研究涉及 PPARγ2 的机制。
给予高脂饮食诱导肥胖的小鼠 120mg/kg/d SY 共 8 周。进行葡萄糖和胰岛素耐量试验。测量脂肪量和血清中葡萄糖和胰岛素的水平。测量脂肪组织中胰岛素信号通路相关基因和 PPARγ2 的表达。体外，还检测了 SY（0-500mg/L）和羟基红花黄色 A（0-100mg/L）对 3T3-L1 前脂肪细胞或脂肪细胞中 PPARγ2 启动子活性和 PPARγ2 信使核糖核酸（mRNA）水平的影响。
红花黄色素降低肥胖小鼠的脂肪量，降低血糖水平并改善胰岛素敏感性。SY 还增加了胰岛素信号通路相关基因的 mRNA 水平，并使皮下脂肪组织中 PPARγ2 mRNA 水平增加了 39.1%（P<0.05）。体外，SY 和羟基红花黄色 A 显著增强了 PPARγ2 启动子活性，使 3T3-L1 前脂肪细胞或脂肪细胞中 PPARγ2 mRNA 水平增加了 1.2-1.6 倍（P<0.05）。
SY 可减少高脂饮食诱导肥胖小鼠的脂肪量，降低血糖水平并改善胰岛素敏感性。其可能的机制是通过刺激 PPARγ2 启动子活性来增加 PPARγ2 的表达，从而进一步增加皮下脂肪组织中胰岛素信号通路相关基因的表达。
