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普洱茶调节高脂饮食小鼠的脂肪酸代谢。

Pu-erh Tea Regulates Fatty Acid Metabolism in Mice Under High-Fat Diet.

作者信息

Huang Fengjie, Wang Shouli, Zhao Aihua, Zheng Xiaojiao, Zhang Yunjing, Lei Sha, Ge Kun, Qu Chun, Zhao Qing, Yan Chao, Jia Wei

机构信息

School of Pharmacy, Shanghai Jiao Tong University, Shanghai, China.

Shanghai Key Laboratory of Diabetes Mellitus and Center for Translational Medicine, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.

出版信息

Front Pharmacol. 2019 Feb 5;10:63. doi: 10.3389/fphar.2019.00063. eCollection 2019.

DOI:10.3389/fphar.2019.00063
PMID:30804786
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6370627/
Abstract

Pu-erh tea has been extensively reported to possess lipid lowering effects but the underlying mechanisms remained unclear. Free fatty acids (FFAs) are generally correlated with the development of obesity, leading to increased risk for type 2 diabetes mellitus and cardiovascular diseases. To investigate whether Pu-erh tea treatment alters FA metabolism, we treated HFD induced obese mice with Pu-erh tea for 22 weeks and analyzed FFA profiles of experimental mice using a UPLC-QTOF-MS platform. Results showed remarkable changes in metabolic phenotypes and FFA compositions in mice treated with or without Pu-erh tea. HFD induced a marked obese phenotype in mice as revealed by significantly increased body weight, liver and adipose tissue weight, lipid levels in serum and liver, and these parameters were markedly reduced by Pu-erh tea treatment. Several FFA or FFA ratios, such as DGLA, palmitoleic acid, and OA/SA ratio, were significantly increased while the levels of SA/PA and AA/DGLA were significantly reduced in HFD-induced obese mice. Interestingly, these differential FFAs or FFA ratios were previous identified as key markers in human obese subjects, and their changes observed in the HFD group were reversed by Pu-erh tea treatment. Moreover, a panel of FFA markers including C20:3 n6/C18:3 n6 and C20:3 n6/C20:2 n6, C18:3 n6/C18:2 n6, C18:3 n3/C18:2 n6 and C24:1 n9/C22:1 n9, which were previously identified as biomarkers in predicting the remission of obesity and diabetes in human subjects who underwent metabolic surgery procedures, were reversed by Pu-erh tea intervention. Pu-erh tea significantly improved glucose homeostasis and insulin tolerance compared to the HFD group. Additionally, Pu-erh tea treatment significantly decreased FFA synthesis genes and increased the expression of genes involved in FFA uptake and β-oxidation including FATP2, FATP5, PPARα, CPT1α, and ACOX-1. These finding confirmed the beneficial effects of Pu-erh tea on regulating lipid and glucose metabolism, and further validated a panel of FFA markers with diagnostic and prognostic value for obesity and diabetes.

摘要

普洱茶已被广泛报道具有降脂作用,但其潜在机制尚不清楚。游离脂肪酸(FFAs)通常与肥胖的发生相关,会增加患2型糖尿病和心血管疾病的风险。为了研究普洱茶处理是否会改变脂肪酸代谢,我们用普洱茶处理高脂饮食诱导的肥胖小鼠22周,并使用超高效液相色谱-四极杆飞行时间质谱平台分析实验小鼠的游离脂肪酸谱。结果显示,在接受或未接受普洱茶处理的小鼠中,代谢表型和游离脂肪酸组成有显著变化。高脂饮食在小鼠中诱导出明显的肥胖表型,表现为体重、肝脏和脂肪组织重量显著增加,血清和肝脏中的脂质水平升高,而普洱茶处理可显著降低这些参数。在高脂饮食诱导的肥胖小鼠中,几种游离脂肪酸或游离脂肪酸比值,如二高-γ-亚麻酸、棕榈油酸和油酸/硬脂酸比值显著增加,而硬脂酸/棕榈酸和花生四烯酸/二高-γ-亚麻酸水平显著降低。有趣的是,这些差异游离脂肪酸或游离脂肪酸比值先前被确定为人类肥胖受试者的关键标志物,在高脂饮食组中观察到的它们的变化被普洱茶处理逆转。此外,一组游离脂肪酸标志物,包括二十碳三烯酸/十八碳三烯酸、二十碳三烯酸/二十碳二烯酸、十八碳三烯酸/十八碳二烯酸、十八碳三烯酸/十八碳二烯酸和二十四碳烯酸/二十二碳烯酸,先前被确定为预测接受代谢手术的人类受试者肥胖和糖尿病缓解的生物标志物,它们的变化被普洱茶干预逆转。与高脂饮食组相比,普洱茶显著改善了葡萄糖稳态和胰岛素耐受性。此外,普洱茶处理显著降低了游离脂肪酸合成基因的表达,并增加了参与游离脂肪酸摄取和β-氧化的基因的表达,包括脂肪酸转运蛋白2、脂肪酸转运蛋白5、过氧化物酶体增殖物激活受体α、肉碱/有机阳离子转运体1α和酰基辅酶A氧化酶-1。这些发现证实了普洱茶对调节脂质和葡萄糖代谢的有益作用,并进一步验证了一组对肥胖和糖尿病具有诊断和预后价值的游离脂肪酸标志物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/efc3/6370627/0fad2033e1af/fphar-10-00063-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/efc3/6370627/dad10727868e/fphar-10-00063-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/efc3/6370627/9b466ece1388/fphar-10-00063-g003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/efc3/6370627/0fad2033e1af/fphar-10-00063-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/efc3/6370627/dad10727868e/fphar-10-00063-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/efc3/6370627/9d87a47c54fd/fphar-10-00063-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/efc3/6370627/9b466ece1388/fphar-10-00063-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/efc3/6370627/5d82232a2219/fphar-10-00063-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/efc3/6370627/0fad2033e1af/fphar-10-00063-g005.jpg

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