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Pharmac Res:喝咖啡或可抑制肥胖相关疾病

首页 » 研究 » 糖尿病 2014-11-17 转化医学网 赞(2)
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来自乔治亚大学的科学家近日通过研究发现,咖啡中的某些常见化合物或可有效帮助抑制肥胖引发的机体损伤效应,相关研究刊登于国际杂志Pharmaceutical Research上。研究者表示,我们发现绿原酸(CGA)可以明显降低高脂肪饮食小鼠胰岛素耐受性及肝脏脂肪的积累。

 来自乔治亚大学的科学家近日通过研究发现,咖啡中的某些常见化合物或可有效帮助抑制肥胖引发的机体损伤效应,相关研究刊登于国际杂志Pharmaceutical Research上。研究者表示,我们发现绿原酸(CGA)可以明显降低高脂肪饮食小鼠胰岛素耐受性及肝脏脂肪的积累。
  此前研究揭示,咖啡的摄入或可降低个体患2型糖尿病及心血管疾病的风险,而本文研究正是基于此来观察咖啡中的特殊化合物对个体机体的有益作用;据美国CDC数据显示,在过去20年间美国的糖尿病患者发病数量急剧增加,超过三分之一的美国成年人及将近17%的儿童都是肥胖个体,而且肥胖的医疗花费超过1470亿美元。
  暂且不说体重会增加,肥胖表现出的两个常见副作用就是胰岛素耐受性的增加及肝脏中脂肪的积累,如果没有得到及时治疗,这些障碍会引发糖尿病和肝功能低下;为了检测绿原酸对小鼠机体的效应,文章中研究者以高脂肪饮食喂养小鼠长达15周时间,同时每周两次对小鼠注射绿原酸,结果显示,绿原酸不仅可以有效抑制小鼠体重增加,而且还可以帮助维持小鼠机体血糖的水平及肝功能的健康。
  研究者Ma说道,绿原酸是一种可以降低炎症的强大抗氧化剂,许多研究证据都显示,肥胖相关的疾病都是由慢性炎症引发的,如果可以及时控制疾病发展,那么或将有效消除过重引发的机体副作用。但研究者同时指出绿原酸并不是万能药,合理的饮食及有规律的锻炼仍然是降低个体肥胖相关疾病风险的最佳方法。
  后期研究人员将继续开展深入研究来开发出改善绿原酸的配方以便人类更好地利用,目前研究者建议人们多饮咖啡来保护机体健康,但是研究人员并不认为他们可以利用绿原酸开发出有效的疗法来帮助改善肥胖个体的相关疾病。(转化医学网360zhyx.com)

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转化医学网推荐的原文摘要:

Chlorogenic Acid Improves High Fat Diet-Induced Hepatic Steatosis and Insulin Resistance in Mice
Pharmaceutical Research doi:10.1007/s11095-014-1526-9
Yongjie Ma, Mingming Gao, Dexi Liu
Purpose
Chlorogenic acid (CGA), the most abundant component in coffee, has exhibited many biological activities. The objective of this study is to assess preventive and therapeutic effects of CGA on obesity and obesity-related liver steatosis and insulin resistance.
Methods
Two sets of experiments were conducted. In set 1, 6-week old C57BL/6 mice were fed a regular chow or high-fat diet (HFD) for 15 weeks with twice intra-peritoneal (IP) injection of CGA (100 mg/kg) or DMSO (carrier solution) per week. In set 2, obese mice (average 50 g) were treated by CGA (100 mg/kg, IP, twice weekly) or DMSO for 6 weeks. Body weight, body composition and food intake were monitored. Blood glucose, insulin and lipid levels were measured at end of the study. Hepatic lipid accumulation and glucose homeostasis were evaluated. Additionally, genes involved in lipid metabolism and inflammation were analyzed by real time PCR.
Results
CGA significantly blocked the development of diet-induced obesity but did not affect body weight in obese mice. CGA treatment curbed HFD-induced hepatic steatosis and insulin resistance. Quantitative PCR analysis shows that CGA treatment suppressed hepatic expression of Pparγ, Cd36, Fabp4, and Mgat1 gene. CGA treatment also attenuated inflammation in the liver and white adipose tissue accompanied by a decrease in mRNA levels of macrophage marker genes including F4/80, Cd68, Cd11b, Cd11c, and Tnfα, Mcp-1 and Ccr2 encoding inflammatory proteins.
Conclusion
Our study provides direct evidence in support of CGA as a potent compound in preventing diet-induced obesity and obesity-related metabolic syndrome. Our results suggest that drinking coffee is beneficial in maintaining metabolic homeostasis when on a high fat diet.


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