Department of Food Science and Nutrition, Kyungpook National University, Daegu 702-701, South Korea.
World J Gastroenterol. 2013 Aug 7;19(29):4689-701. doi: 10.3748/wjg.v19.i29.4689.
To investigate long-term effects of Garcinia Cambogia (GC), weight-loss supplement, on adiposity and non-alcoholic fatty liver disease in obese mice.
Obesity-prone C57BL/6J mice were fed a high-fat diet (HFD, 45 kcal% fat) with or without GC (1%, w/w) for 16 wk. The HFD contained 45 kcal% fat, 20 kcal% protein and 35 kcal% carbohydrate. They were given free access to food and distilled water, and food consumption and body weight were measured daily and weekly, respectively. Data were expressed as the mean ± SE. Statistical analyses were performed using the statistical package for the social science software program. Student's t test was used to assess the differences between the groups. Statistical significance was considered at P < 0.05.
There were no significant changes in body weight and food intake between the groups. However, the supplementation of GC significantly lowered visceral fat accumulation and adipocyte size via inhibition of fatty acid synthase activity and its mRNA expression in visceral adipose tissue, along with enhanced enzymatic activity and gene expression involved in adipose fatty acid β-oxidation. Moreover, GC supplementation resulted in significant reductions in glucose intolerance and the plasma resistin level in the HFD-fed mice. However, we first demonstrated that it increased hepatic collagen accumulation, lipid peroxidation and mRNA levels of genes related to oxidative stress (superoxide dismutase and glutathione peroxidase) and inflammatory responses (tumor necrosis factor-α and monocyte chemoattractant protein-1) as well as plasma alanine transaminase and aspartate transaminase levels, although HFD-induced hepatic steatosis was not altered.
GC protects against HFD-induced obesity by modulating adipose fatty acid synthesis and β-oxidation but induces hepatic fibrosis, inflammation and oxidative stress.
研究 Garcinia Cambogia(GC),一种减肥补充剂,对肥胖小鼠的肥胖和非酒精性脂肪性肝病的长期影响。
将肥胖易感的 C57BL/6J 小鼠用高脂肪饮食(HFD,45%热量脂肪)喂养,并用或不用 GC(1%,w/w)喂养 16 周。HFD 含有 45%热量脂肪、20%热量蛋白质和 35%热量碳水化合物。它们可以自由食用食物和蒸馏水,分别每天和每周测量食物摄入量和体重。数据表示为平均值±SE。使用社会科学软件程序的统计包进行统计分析。使用学生 t 检验评估组间差异。P<0.05 被认为具有统计学意义。
体重和食物摄入量在各组之间没有显著变化。然而,GC 的补充通过抑制内脏脂肪组织中脂肪酸合酶活性及其 mRNA 表达,同时增强脂肪脂肪酸β-氧化相关的酶活性和基因表达,显著降低了内脏脂肪的积累和脂肪细胞的大小。此外,GC 补充可显著降低 HFD 喂养小鼠的葡萄糖不耐受和血浆抵抗素水平。然而,我们首先证明它增加了肝胶原积累、脂质过氧化以及与氧化应激(超氧化物歧化酶和谷胱甘肽过氧化物酶)和炎症反应(肿瘤坏死因子-α和单核细胞趋化蛋白-1)相关的基因的 mRNA 水平以及血浆丙氨酸转氨酶和天冬氨酸转氨酶水平,尽管 HFD 诱导的肝脂肪变性没有改变。
GC 通过调节脂肪脂肪酸的合成和β-氧化来预防 HFD 诱导的肥胖,但会引起肝纤维化、炎症和氧化应激。