Abstract
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.
Highlights
Obesity has become one of the most challenging health problems in the twenty-first century
The body weight of the mice in high-fat diet (HFD) significantly increased compared with mice fed in the ND group (p < 0.01), but curcumin (50 mg kg−1 d−1) supplement markedly reduced body weight starting from the third week
The fat mass grew to 0.43 ± 0.02 and 0.35 ± 0.02 at week 8, respectively. These results indicated that HFD effectively induced obesity and curcumin could reduce body weight and fat mass in HFD-induced obese mice
Summary
Obesity has become one of the most challenging health problems in the twenty-first century. The latest statistics showed that more than 1.0 billion adults worldwide were overweight; of these, over 400 million were obese [1]. It is usually accompanied with complex metabolic disorders, and significantly increases the risk of several common and serious diseases such as diabetes mellitus, hyperlipidaemia, hypertension, cardiovascular disease and non-alcoholic fatty liver disease [2]. Obesity is characterized by excessive accumulation of body fat (triglycerides (TGs)) in adipose tissue [3]. Dysfunction or excessive adipose storage of adipose tissue may lead to ectopic lipid accumulation and lipotoxicity in obese individuals and block insulin signalling transport [6,7]
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