Curcumin improves glycolipid metabolism through regulating peroxisome proliferator activated receptor γ signalling pathway in high-fat diet-induced obese mice and 3T3-L1 adipocytes.
Yan-Yun PanDandan ZhaoNa YuTian AnJianan MiaoFangfang MoYujie GuDongwei ZhangSihua GaoGuangjian JiangPublished in: Royal Society open science (2017)
Curcumin is an active component derived from Curcuma longa L. which is a traditional Chinese medicine that is widely used for treating metabolic diseases through regulating different molecular pathways. Here, in this study, we aimed to comprehensively investigate the effects of curcumin on glycolipid metabolism in vivo and in vitro and then determine the underlying mechanism. Male C57BL/6 J obese mice and 3T3-L1 adipocytes were used for in vivo and in vitro study, respectively. Our results demonstrated that treatment with curcumin for eight weeks decreased body weight, fat mass and serum lipid profiles. Meanwhile, it lowered fasting blood glucose and increased the insulin sensitivity in high-fat diet-induced obese mice. In addition, curcumin stimulated lipolysis and improved glycolipid metabolism through upregulating the expressions of adipose triglyceride lipase and hormone-sensitive lipase, peroxisome proliferator activated receptor γ/α (PPARγ/α) and CCAAT/enhancer binding proteinα (C/EBPα) in adipose tissue of the mice. In differentiated 3T3-L1 cells, curcumin reduced glycerol release and increased glucose uptake via upregulating PPARγ and C/EBPα. We concluded that curcumin has the potential to improve glycolipid metabolism disorders caused by obesity through regulating PPARγ signalling pathway.
Keyphrases
- high fat diet induced
- insulin resistance
- adipose tissue
- blood glucose
- high fat diet
- metabolic syndrome
- binding protein
- skeletal muscle
- glycemic control
- body weight
- type diabetes
- fatty acid
- induced apoptosis
- body mass index
- blood pressure
- cell proliferation
- weight loss
- transcription factor
- cell death
- single molecule
- signaling pathway
- low density lipoprotein
- cell cycle arrest