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桦木酸通过激活 AMPK 抑制高脂肪饮食诱导的肥胖并改善能量平衡。

Betulinic acid inhibits high-fat diet-induced obesity and improves energy balance by activating AMPK.

机构信息

School of Life Science, Handong Global University, Pohang, Gyungbuk, South Korea.

Division of Integrative Biosciences and Biotechnology, POSTECH, Pohang, Gyungbuk, South Korea; R&D Center, NovMetaPharma Co., Ltd., Pohang, Gyungbuk, South Korea.

出版信息

Nutr Metab Cardiovasc Dis. 2019 Apr;29(4):409-420. doi: 10.1016/j.numecd.2018.12.001. Epub 2019 Jan 8.

DOI:10.1016/j.numecd.2018.12.001
PMID:30799179
Abstract

BACKGROUND AND AIM

Metabolic syndromes are prevalent worldwide and result in various complications including obesity, cardiovascular disease and type II diabetes. Betulinic acid (BA) is a naturally occurring triterpenoid that has anti-inflammatory properties. We hypothesized that treatment with BA may result in decreased body weight gain, adiposity and hepatic steatosis in a diet-induced mouse model of obesity.

METHODS AND RESULTS

Mice fed a high-fat diet and treated with BA showed less weight gain and tissue adiposity without any change in calorie intake. Gene expression profiling of mouse tissues and cell lines revealed that BA treatment increased expression of lipid oxidative genes and decreased that of lipogenesis-related genes. This modulation was mediated by increased AMP-activated protein kinase (AMPK) phosphorylation, which facilitates energy expenditure, lipid oxidation and thermogenic capacity and exerts protective effects against obesity and nonalcoholic fatty liver disease. Overall, BA markedly inhibited the development of obesity and nonalcoholic fatty liver disease in mice fed a high-fat diet, and AMPK activation in various tissues and enhanced thermogenesis are two possible mechanisms underlying the antiobesity and antisteatogenic effects of BA.

CONCLUSIONS

The current findings suggest that treatment with BA is a potential dietary strategy for preventing obesity and nonalcoholic fatty liver disease.

摘要

背景与目的

代谢综合征在全球范围内普遍存在,并导致各种并发症,包括肥胖、心血管疾病和 2 型糖尿病。白桦脂酸(BA)是一种天然存在的三萜类化合物,具有抗炎特性。我们假设 BA 的治疗可能会导致肥胖症小鼠模型中体重增加、肥胖和肝脂肪变性减少。

方法和结果

给予高脂肪饮食的小鼠用 BA 治疗后,体重增加和组织肥胖减少,而热量摄入没有变化。对小鼠组织和细胞系的基因表达谱分析显示,BA 处理增加了脂质氧化基因的表达,减少了与脂生成相关的基因的表达。这种调节是通过增加 AMP 激活的蛋白激酶(AMPK)磷酸化介导的,这有助于能量消耗、脂质氧化和产热能力,并对肥胖和非酒精性脂肪肝发挥保护作用。总的来说,BA 显著抑制了高脂肪饮食喂养的小鼠肥胖和非酒精性脂肪肝的发展,而 AMPK 在各种组织中的激活和增强的产热是 BA 具有抗肥胖和抗脂肪变性作用的两个可能机制。

结论

目前的研究结果表明,BA 的治疗可能是预防肥胖和非酒精性脂肪肝的一种潜在饮食策略。

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