Effect of Garcinia cambogia extract on adipogenesis reduction

• Main Authors: Yu-Ying Chu, 朱育瑩
• Other Authors: 顏國欽
• Format: Others
• Language: zh-TW
• Published: 2011
• Online Access: http://ndltd.ncl.edu.tw/handle/45334291399742117401

碩士 === 國立中興大學 === 食品暨應用生物科技學系所 === 99 === Obesity is becoming a major public health problem in many parts of the world. It is a significant risk factor for various diseases such as type 2 diabetes mellitus, cardiovascular disease, fatty liver and cancer. The major cause of obesity is mainly long-term higher energy intake than energy expenditure, resulting in the body fat accumulation. Hydroxycitric acid (HCA) isolated from the fruit rind of Garcinia cambogia has been shown inhibiting ATP citrate lyase (ACL) activity, decreasing serum leptin concentration but increasing brain release serotonin to suppress appetite. However, the effects of HCA on modulation of transcription factors and downstream adipokines expressions in 3T3-L1 preadipocytes during differentiation have not yet been investigated. Furthermore, it is not clear the effect of Garcinia cambogia extract (GCE) on adipogenesis reduction after several food processing. First, we investigated the effect of HCA on modulation of transcription factors and adipokine expressions in 3T3-L1 preadipocytes during differentiation. The results showed that HCA at 50 μM inhibited fat droplet formation and significantly (p＜0.05) decreased intracellular triglycerol accumulation. For the activities of ACL and carnitine palmitoyltransferase 1 (CPT1), these data indicated that ACL activity was decreased but CPT1 activity was increased (p＜0.05) by HCA treatment. HCA had anti-adipogenesis effect by suppressing the mRNA expressions of PPARγ, C/EBPα, FAS and LPL. Morerover, HCA inhibited the adipokines such as leptin and resistin but up-regulated the mRNA expression of adiponectin. The protein expressions of PPARγand C/EBPα were decreased, but adiponectin was increased by HCA treatment (p＜0.05). We further examined the effect of GCE on adipogenesis reduction at the low and high doses (300 and 600 mg/kg B.W., respectively) by pretreating with acidification (pH 4.3) and heating (121°C, 15 mins) (AL and AH) or without acidification and heating (NL and NH) in an animal model of high-fat diet (HFD)-induced obesity. The animals were fed AL, AH, NL or NH for a period of 8 weeks. The results showed that the 45% of HCA was converted into hydroxycitric acid lactone (HCAL) after acidification and heating. Body weight, adipose tissue weight and body fat ratio in HFD+AL, HFD+AH and HFD+NH groups were significantly (p<0.05) decreased as compared to the HFD group. A significant (p<0.05) decrease in the serum triacylglycerol, total cholesterol, LDL-cholesterol and glucose was observed in HFD+AL, HFD+AH and HFD+NH groups as compared with the HFD group. Histological study showed that the lipid droplets in HFD+AL, HFD+AH and HFD+NH groups were less than the HFD group. Liver triacylgiycerol level in HFD+AL, HFD+AH and HFD+NH groups were also significantly (p<0.05) decreased as compared with the HFD group. Moreover, the AL, AH and NH treated group decreased ACL activity, but increased (p<0.05) CPT1 activity in the hepatic tissue of rats with HFD-induced obesity. In conclusion, HCA can inhibit adipogenesis and regulate adipokines in 3T3-L1 preadipocytes during differentiation. Administration of GCE could be beneficial to the suppression of HFD-induced dyslipidemia, hepatosteatosis and reduced adipogenesis in SD rats. Furthermore, the GCE pretreating with acidification and heating might be useful to the development of functional food for the adipogenesis reduction of body fat.