茶葉調(diào)節(jié)SREBPs的降脂作用

潘聯(lián)云，鹿顏，龔雨順

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茶葉調(diào)節(jié)SREBPs的降脂作用

潘聯(lián)云，鹿顏，龔雨順*

湖南農(nóng)業(yè)大學(xué)園藝園林學(xué)院，國家植物功能成分利用工程技術(shù)研究中心，茶學(xué)教育部重點(diǎn)實(shí)驗室，湖南省植物功能成分利用協(xié)同創(chuàng)新中心，湖南 長沙 410128

茶葉可調(diào)節(jié)不同組織的脂質(zhì)代謝，抑制腸道消化吸收脂質(zhì)，起到降脂減肥作用。茶葉對脂質(zhì)代謝途徑具有顯著影響，主要通過調(diào)控固醇調(diào)節(jié)元件結(jié)合蛋白（Sterol Regulatory Element Binding Proteins）及其上下游因子表達(dá)，影響脂質(zhì)合成和分解，從而降低脂肪積累。

茶；肥胖；脂質(zhì)代謝；SREBP

肥胖與糖尿病、高脂血癥、動脈粥樣硬化和某些癌癥等密切相關(guān)[1-2]。茶葉可以調(diào)控脂質(zhì)代謝途徑中的關(guān)鍵基因或限制酶，如（同源哺乳動物）或硬脂酰輔酶A去飽和酶（Stearyol-Co A desaturase, SCD），降低肥胖和相關(guān)疾病發(fā)生率[3-7]。探索茶葉降脂作用及其功能機(jī)理，有利于深入研究茶葉的保健功能。

1 茶葉降脂研究現(xiàn)狀

流行病學(xué)研究表明，茶葉具有降脂減肥作用[8-9]，長期喝茶人群的脂肪堆積明顯降低，腰、臀圍比顯著下降[10]。茶葉及茶葉生物活性成分（茶多酚和兒茶素等）可以降低體重、減少脂肪含量、抑制高血脂癥與糖尿病、降低動脈粥樣硬化指數(shù)、促進(jìn)低密度脂蛋白受體表達(dá)，以及降低血漿甘油三酯、膽固醇和低密度脂蛋白水平[11-13]。

1.1 茶葉降低脂肪含量

綠茶可以降低Wistar大鼠脂肪組織總重量，不影響肌肉組織和結(jié)蹄組織重量[14]。普洱茶可以降低C57BL/6J小鼠脂肪含量[15]，改變秀麗線蟲脂滴的大小和數(shù)量[16]。茯磚茶特有的冠突散囊菌提取液能夠降低3T3-L1脂肪細(xì)胞和秀麗線蟲的脂質(zhì)含量，抑制脂肪沉積[17]。除此之外，紅茶和烏龍茶也能夠降低C57BL/6J小鼠內(nèi)臟脂質(zhì)積累[18]。

1.2 茶葉調(diào)節(jié)肝臟、胰臟、骨骼肌和脂肪組織的脂質(zhì)代謝

茶葉提取物能夠促進(jìn)肝臟脂肪氧化，減少脂肪和葡萄糖生成；增加肌肉組織對葡萄糖吸收和促進(jìn)脂肪氧化，提高線粒體的生物合成，促進(jìn)有氧呼吸和代謝作用；提高脂肪組織胰島素敏感性，降低脂質(zhì)合成和分解代謝，減少異位脂肪沉積，減少肥胖的發(fā)生[19-21]。此外，茶葉還可以調(diào)控胰臟減少胰島素分泌，降低胰島素水平、降低脂質(zhì)合成[22]（圖1）。

不同茶類調(diào)節(jié)肝臟、胰臟、骨骼肌和脂肪組織的脂質(zhì)代謝機(jī)制各不相同。綠茶含有豐富的兒茶素、茶氨酸和咖啡堿等物質(zhì)，可以促進(jìn)肝臟和骨骼肌脂肪酸的β氧化和生熱作用[23-26]，可提高血清脂聯(lián)素合成[27-29]，還能降低脂肪組織的脂質(zhì)合成、吸收和沉積[30-31]。紅茶的大分子多酚可以通過抑制胰臟分脂肪酶來減少脂質(zhì)吸收[18,32]。烏龍茶降脂機(jī)制和紅茶相似，烏龍茶含有聚酯型兒茶素，能夠促進(jìn)去甲腎上腺素分泌和抑制胰脂肪酶活性，從而提高脂質(zhì)分解和減少脂肪吸收[18,33]。

1.3 茶葉抑制脂質(zhì)消化吸收

茶葉通過影響脂質(zhì)乳化、消化和膠束增溶作用干擾腸道吸收脂質(zhì)（圖1）。通過研究體外細(xì)胞和高血脂、動脈粥樣硬化的大鼠[34-35]，以及進(jìn)行大鼠腸系膜淋巴管插管實(shí)驗[34, 36-38]，發(fā)現(xiàn)綠茶及其活性成分兒茶素，尤其是表沒食子兒茶素沒食子酸酯（(-)-Epigallocatechin gallate, EGCG），可以影響脂質(zhì)乳化、消化和膠束增溶作用，阻礙腸道脂質(zhì)吸收和肝臟脂肪生成[20,39]。茶多酚可以通過氫鍵和疏水鍵與消化蛋白酶和蛋白質(zhì)進(jìn)行結(jié)合，降低消化系統(tǒng)對營養(yǎng)物質(zhì)的吸收作用[22]。紅茶中茶多酚和EGCG能夠干擾脂肪乳化，抑制哺乳動物磷脂酶和胰脂肪酶的活性，降低脂質(zhì)吸收[31, 40-41]。

以秀麗線蟲為模型，通過喂食GFP-OP50（帶有綠色熒光的大腸桿菌）觀察普洱茶對線蟲飲食的影響，結(jié)果發(fā)現(xiàn)飲用普洱茶的實(shí)驗組，其咽泵運(yùn)動頻率和腸道熒光強(qiáng)度都明顯降低[16]。一種特殊的發(fā)酵綠茶可以改變大鼠腸道厚壁菌/擬桿菌和擬桿菌/普氏菌的比率，降低肥胖發(fā)生和脂肪肝形成[42]。

圖1 茶葉在組織和器官中的作用

綜上所述，未發(fā)酵茶、發(fā)酵茶和微生物發(fā)酵茶均能降低脂肪含量。但不同類型的茶或者來自不同地方同一類型的茶，其降脂減肥機(jī)制和作用效果各不相同；同一種茶的不同成分作用效果也各不相同。增強(qiáng)脂質(zhì)氧化、提高能量消耗或減少食物攝入、抑制脂肪和營養(yǎng)物質(zhì)吸收是茶葉降脂減肥作用的關(guān)鍵。

2 茶葉調(diào)節(jié)脂肪相關(guān)因子SREBP研究現(xiàn)狀

在生物生命活動中，脂肪酸合成、轉(zhuǎn)運(yùn)和氧化，糖酵解和糖異生等過程都能影響脂質(zhì)積累[43]。近期研究發(fā)現(xiàn)，茶葉對脂質(zhì)代謝SREBP途徑具有顯著影響，茶葉活性成分通過調(diào)節(jié)SREBP及其上游元件（AMPK、PPARγ、FXR與LXR）和下游元件（ACC、FAS、SCD、HMGCR、GPAT與FAT-5/6/7）來抑制脂肪生成，降低脂肪酸不飽和度，減少生物自身脂肪積累[44-46]（圖2）。

2.1 脂質(zhì)代謝因子SREBP概述

SREBP屬于堿性螺旋-環(huán)-螺旋亮氨酸拉鏈轉(zhuǎn)錄因子家族，是真核生物調(diào)節(jié)脂質(zhì)合成的關(guān)鍵核轉(zhuǎn)錄因子。未活化的SREBP前體先在內(nèi)質(zhì)網(wǎng)上合成，然后經(jīng)過第1位點(diǎn)蛋白酶（Site 1 protease, S1P）和第2位點(diǎn)蛋白酶（Site 2 protease, S2P）的兩次裂解活化，成為成熟核型SREBP（n-SREBP），最后轉(zhuǎn)移到細(xì)胞核內(nèi)，與靶基因（脂肪酸、膽固醇代謝基因和SREBP）啟動子/增強(qiáng)子的固醇調(diào)節(jié)元件（Sterol response element, SRE）或E-box結(jié)合激活轉(zhuǎn)錄[47]。SREBP有3種亞型：包括同一基因編碼、通過選擇性剪切形成的兩個亞型SREBP-1c和SREBP-1a，以及由另1個獨(dú)立基因編碼的SREBP-2亞型[48-49]。

注：→：激活、促進(jìn)或正調(diào)控；：抑制或負(fù)調(diào)控；：SREBP合成和降解。UPS：泛素－蛋白酶體系統(tǒng)；AA：氨基酸。

無脊椎動物與哺乳動物中脂肪的合成、分化都需要SREBP參與，SREBP與脂質(zhì)代謝轉(zhuǎn)錄調(diào)節(jié)因子的輔因子MDT-15相互作用，調(diào)節(jié)脂肪酸與膽固醇生成和轉(zhuǎn)運(yùn)[50-51]。SREBP-1c主要調(diào)控脂肪酸合成途徑的基因表達(dá)，SREBP-2主要調(diào)控膽固醇合成途徑的基因表達(dá)以及低密度脂蛋白受體基因表達(dá)，SREBP-1a則是全身性低水平行使以上兩種亞型的功能[15-16, 52]。SREBPRNAi或SREBP功能缺失的生物會出現(xiàn)生長延遲、脂肪含量降低、腸道脂滴減少和脂肪合成基因（和）表達(dá)量下降等現(xiàn)象[53-54]。

2.2 茶葉對SREBP的調(diào)節(jié)機(jī)制

2.2.1 茶葉對SREBP-1c下游因子的調(diào)節(jié)機(jī)制

SREBP-1c是乙酰輔酶A羧化酶（Acetyl-CoA carboxylase, ACC）、脂肪酸合成酶（Fatty acid synthetase, FAS）、SCD、脂肪酸延伸酶（Fatty acids extends enzyme, FAE）和甘油脂酰轉(zhuǎn)移酶（Glycerol phosphate acyltransferase, GPAT）的上游因子[15,55]。茶葉提取物能夠影響SREBP-1c表達(dá)、降低甘油三酯含量、刺激脂質(zhì)氧化分解，且呈劑量依賴性趨勢[15,55-56]。在分化的脂肪前體細(xì)胞中，0.5%白茶提取物能夠降低SREBP-1c的mRNA與蛋白表達(dá)水平，抑制脂肪合成[56-57]。茶葉提取物特別是EGCG通過下調(diào)脂肪生成基因的表達(dá)來抑制脂肪生成[3,58-59]。EGCG能夠下調(diào)H4IIE大鼠肝癌細(xì)胞中FAS和SCD的mRNA表達(dá)水平[60]。相比對照組，含有1.0% EGCG的高脂飲食的實(shí)驗組C57BL/6J小鼠血漿中甘油三酯的含量明顯降低，脂肪酸合成限速酶基因（ACC, SCD和FAS等）表達(dá)顯著下調(diào)[61]。

此外，正常培養(yǎng)條件下茶葉提取物下調(diào)秀麗隱桿線蟲SBP-1（同源哺乳動物SREBP）的表達(dá)，從而抑制其靶目標(biāo)基因SCD活性，導(dǎo)致脂肪儲存下降[16]。在高脂飲食條件下，茶葉活性成分能夠降低C57BL/6J小鼠脂肪酶mRNA表達(dá)，抑制脂肪和膽汁酸積累，影響糞便總膽固醇的含量[15]。在高葡萄糖環(huán)境中，綠茶和紅茶都會增加脂肪酸合成酶（SREBP-1c, FAS, ACC）和氧化酶（PPAR-α, CPT-1, ACO）的表達(dá)，促進(jìn)肝臟脂肪合成和分解，提高脂質(zhì)代謝，抑制脂肪分化，抑制脂肪組織吸收脂肪酸，降低脂肪和葡萄糖積累，減少葡萄糖的毒害作用和提高機(jī)體對葡萄糖的耐受性[50,62]。高果糖飲食增加大鼠肝臟SREBP-1c、FAS和SCD1的mRNA表達(dá)，通過長期飲茶處理，這些基因的表達(dá)顯著下調(diào)[20,63-64]。

2.2.2 茶葉對SREBP-2下游因子的調(diào)節(jié)機(jī)制

低密度脂蛋白受體（Low density lipoprotein receptor, LDLR）和羥甲基戊二酸單酰輔酶A還原酶（3-hydroxy-3-methyl glutaryl coenzyme A reductase, HMGCR）是SREBP-2下游因子，主要參與調(diào)控膽固醇的合成和轉(zhuǎn)運(yùn)[15,55]。LDLR是清除低密度脂蛋白的跨膜受體，HMGCR是膽固醇生物合成的第一步限速酶。普洱茶通過競爭性抑制HMGCR減少細(xì)胞膽固醇合成，從而反饋刺激LDLR數(shù)量和活性增加，促進(jìn)血清膽固醇清除[15,65-67]。綠茶及其活性成分茶多酚可以作為一種蛋白酶體抑制劑，抑制HepG2和HeLa活化的SREBP-2泛素化-蛋白質(zhì)降解，促進(jìn)LDLR表達(dá)[68-69]。高脂飲食的實(shí)驗組C57BL/6J小鼠飲用普洱茶70?d后，HMGCR的mRNA表達(dá)水平顯著下調(diào)，且呈劑量依賴性趨勢[15]。

2.2.3 茶葉對SREBP上游因子的調(diào)節(jié)機(jī)制

腺苷酸活化蛋白激酶（Adenosine 5′-monophosphate (AMP)-activated protein kinase, AMPK）、肝臟X活化受體（Liver X-activated receptor, LXR）、FXR（法尼酯衍生物X受體）和過氧化氫酶體增殖激活受體（Peroxisome proliferator-activated receptor, PPAR）是SREBP的上游因子，茶葉可以通過調(diào)控這些基因來間接調(diào)節(jié)SREBP轉(zhuǎn)錄和蛋白剪切，從而調(diào)控脂肪酸和膽固醇的生物合成。

AMPK是調(diào)節(jié)生物能量代謝的關(guān)鍵因子，作為能量調(diào)節(jié)開關(guān)，AMPK在脂質(zhì)代謝中發(fā)揮著重要作用[70-72]。綠茶EGCG可以通過瘦素和脂聯(lián)素等肽類激素介導(dǎo)的AMP非依賴通路或AMPK上游激酶，如肝激酶B1（Liver kinase B1, LKB1），激活A(yù)MPK磷酸化[27]。磷酸化AMPK增加其下游分子PPARγ的磷酸化水平，降低SREBP活性，進(jìn)而下調(diào)ACC和HMGCR表達(dá)，導(dǎo)致脂肪合成和轉(zhuǎn)運(yùn)下降，脂肪沉積減少[70,73-76]；同時，AMPK磷酸化可以進(jìn)一步促進(jìn)其下游分子PPARα和脂蛋白脂酶（Lipoprotein lipase, LPL）活性，增強(qiáng)脂肪分解代謝[48-49]。綠茶多酚可以通過抑制細(xì)胞外調(diào)節(jié)蛋白激酶（Eextracellular regulated protein kinases, ERK-1/2）活性降低PPARγ磷酸化，增加PPARγ表達(dá)，促進(jìn)脂聯(lián)素合成[29]，而脂聯(lián)素能夠降低高脂飲食小鼠體重和血糖水平、提高胰島素敏感性、刺激AMPK磷酸化[27]。

EGCG能顯著激活FXR，從而抑制SREBP-1c和促進(jìn)PPARα表達(dá)來降低甘油三酯合成[77]。綠茶茶多酚上調(diào)PPARα基因表達(dá)促進(jìn)脂肪氧化，同時下調(diào)LXR和PPARγ基因表達(dá)降低SREBP-1c轉(zhuǎn)錄，從而抑制動脈粥樣硬化變病[69]。

此外，胰島素能夠提高SREBP mRNA和前體蛋白水平，以及促進(jìn)SREBP蛋白的剪切加工[47]。綠茶及其活性物質(zhì)茶多酚上調(diào)胰島素受體底物（Insulin receptor substrate, IRS）水平，提高哺乳動物胰島素敏感性，抑制胰臟釋放胰島素，從而下調(diào)SREBP mRNA和蛋白水平，減少脂質(zhì)合成[31,78-79]。茶葉還能夠下調(diào)轉(zhuǎn)錄調(diào)節(jié)因子輔因子MDT-15，抑制固醇調(diào)節(jié)元件結(jié)合蛋白SREBP、核激素受體NHR-49和核轉(zhuǎn)錄因子SKN-1（同源哺乳動物Nrf2）與其結(jié)合，從而降低脂肪酸合成[51,53]。

2.2.4 茶葉通過調(diào)節(jié)SREBP改變脂肪酸組成成分

軟脂酸（C16:1）和油酸（C18:1n-9）是主要單不飽和脂肪酸，也是甘油三酯、磷脂質(zhì)、膽固醇酯的生物合成重要前體物質(zhì)[80-81]。茶葉提取物能夠增加硬脂酸（C18:0）含量，顯著降低不飽和脂肪酸油酸和亞麻酸（C18:2）的儲存水平[82]。

在飽和脂肪酸（C16:0和C18:0）轉(zhuǎn)化為不飽和脂肪酸（C16:1n-7和C18:1n-9）的過程中，SCD能夠促進(jìn)C9和C10之間雙鍵生成，催化飽和脂肪酸去飽和化[83]。茶葉活性成分可以降低小鼠SCD-1 mRNA表達(dá)，增加飽和脂肪酸含量[16]。普洱茶下調(diào)C57BL/6J小鼠和秀麗隱桿線蟲的SREBP/SBP-1及其相關(guān)作用元件如MDT-15的表達(dá)，抑制脂質(zhì)合成過程中關(guān)鍵酶SCD的活性，降低硬脂酸去飽和化，從而導(dǎo)致脂質(zhì)儲存下降[15-16,84]。普洱茶還能夠下調(diào)編碼SCD蛋白的基因（），降低SCD含量，減少脂質(zhì)積累[85-86]。此外，茶提取物也會下調(diào)和來降低油酸/硬脂酸的比率[87-89]。

3 結(jié)論

綜上所述，茶葉的降脂作用機(jī)制主要通過調(diào)節(jié)脂質(zhì)代謝關(guān)鍵轉(zhuǎn)錄因子SREBP來實(shí)現(xiàn)降脂減肥作用。

茶多酚、咖啡堿和茶氨酸是茶葉降脂減肥的主要活性成分，能夠有效抑制脂質(zhì)積累和降低脂肪含量。茶葉及其活性成分降脂減肥的機(jī)制如下：（1）抑制脂肪前體細(xì)胞增殖；（2）誘導(dǎo)脂肪前體細(xì)胞和成熟脂肪細(xì)胞凋亡；（3）抑制脂肪前體細(xì)胞分化和成熟脂肪細(xì)胞生成；（4）抑制腸胃消化酶活性，干擾脂質(zhì)乳化、水解和膠束增溶作用；（5）干擾腸道乳糜微粒的裝配和分泌，阻礙脂質(zhì)吸收和運(yùn)輸；（6）抑制胰臟分泌胰脂肪酶，減少脂質(zhì)吸收；（7）增加糞便排泄物脂質(zhì)含量和全氮含量；（8）改變腸道微生物菌群，影響營養(yǎng)物質(zhì)吸收；（9）促進(jìn)脂聯(lián)素合成，提高胰島素敏感性，降低胰島素分泌水平；（10）下調(diào)肝臟脂肪和糖原合成基因與相關(guān)轉(zhuǎn)錄因子，提高肝臟脂肪酸的β氧化基因mRNA水平；（11）促進(jìn)骨骼肌脂肪酸的氧化和葡萄糖的吸收；（12）提高脂肪組織的脂肪酸氧化和脂質(zhì)分解基因表達(dá)，抑制脂肪組織葡萄糖吸收和脂肪合成相關(guān)因子表達(dá)；（13）調(diào)節(jié)脂質(zhì)合成基因表達(dá)，改變脂肪酸組分。

SREBP的mRNA表達(dá)、蛋白剪切、加工和降解均與脂質(zhì)代謝密切相關(guān)。在SREBP脂質(zhì)代謝途徑中，茶葉及其活性成分即可直接抑制SREBP，也可通過上調(diào)AMPK和FXR或下調(diào)PPARγ、LXR和MDT-15表達(dá)來間接抑制SREBP。茶葉提取物通過提高AMPK磷酸化、激活FXR、下調(diào)LXR和PPARγ來下調(diào)SREBP mRNA表達(dá)或抑制SREBP蛋白活性。同時，茶葉提取物也可以通過抑制ERK-1/2提高PPARγ表達(dá)，促進(jìn)脂聯(lián)素合成，繼而刺激AMPK磷酸化，抑制PPARγ表達(dá)，從而降低SREBP活性，因此ERK-1/2和AMPK途徑相互抑制又相互依賴。

茶葉活性物質(zhì)還能夠通過促進(jìn)脂聯(lián)素合成或者上調(diào)IRS來提高胰島素敏感性，降低胰島素水平，抑制SREBP表達(dá)。茶葉活性物質(zhì)還能夠通過下調(diào)SREBP的轉(zhuǎn)錄調(diào)節(jié)因子輔因子來降低SREBP水平。

脂肪酸合成酶（SREBP-1c、ACC、SCD和FAS等）和氧化酶（PPAR-α、CPT-1、ACO）基因是調(diào)節(jié)脂肪酸合成和脂質(zhì)積累的重要因子。正常情況下，茶葉提取物下調(diào)脂肪酸合成酶基因，上調(diào)氧化酶基因，提高脂質(zhì)分解，減少脂肪酸合成，降低脂肪含量。在高糖條件下，為了減少高糖對生物體的毒害作用，茶葉提取物能夠同時提高脂質(zhì)合成和氧化基因表達(dá)，促進(jìn)糖異生作用，增加脂肪酸氧化分解，降低脂質(zhì)，提高葡萄糖耐受性。當(dāng)SREBP-1c活性降低則會進(jìn)一步降低脂肪酸合成酶基因FAS、ACC、SCD、CPAT、HMGCR、FAT-5/6/7和LDLR的表達(dá)，導(dǎo)致甘油三酯含量下降、脂質(zhì)積累降低。據(jù)研究，茶葉對SREBP-2下游因子LDLR和HMGCR具有調(diào)控作用。茶葉提取物能夠抑制活化的SREBP-2降解，提高LDLR表達(dá)，清除多余的膽固醇；相反，抑制未活化的SREBP-2表達(dá)，可以下調(diào)HMGCR mRNA水平，減少膽固醇合成。此外，茶葉還能夠競爭性抑制HMGCR表達(dá)，反饋調(diào)節(jié)LDLR活性，進(jìn)而調(diào)節(jié)膽固醇的合成和轉(zhuǎn)運(yùn)。

肥胖發(fā)生不僅取決于脂肪含量，還取決于脂肪酸的組成成分，特別是多不飽和脂肪酸（Polyunsaturated Fatty Acids, PUFAs）的組分，如ω-3 PUFAs可以通過抑制腸道吸收甘油三酯和肝臟合成內(nèi)源甘油三酯等途徑降低血漿甘油三酯水平。茶葉提取物通過抑制SREBP表達(dá)，下調(diào)ACC、FAS、FAE和SCD表達(dá)，從而分別抑制乙酰輔酶A轉(zhuǎn)化、飽和脂肪酸合成、延伸和去飽和化，繼而影響脂肪酸組成成分。

茶葉可通過多條途徑和多個作用位點(diǎn)調(diào)控脂質(zhì)代謝，不同茶葉對脂質(zhì)代謝調(diào)控作用機(jī)制不同，其效果也不同。據(jù)統(tǒng)計，研究茶葉降脂減肥機(jī)制以綠茶為主，而紅茶、烏龍茶、黑茶和普洱茶研究仍然較少。自然環(huán)境的不可控性、制茶工藝的多樣性、茶葉活性成分的不穩(wěn)定性、脂質(zhì)代謝機(jī)制的復(fù)雜性限制了我們對茶葉降脂減肥機(jī)制的研究。因此茶葉降脂減肥機(jī)制還需要從多方面深入研究探索。

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The Mechanism of the Lipid-lowering Effect of Tea by Regulating the SREBP

PAN Lianyun, LU Yan, GONG Yushun*

Hunan Agricultural University, College of Horticulture and Landscape, National Engineering Center of Plant Functional Components Utilization, Key Lab of Tea Science, Hunan Co-Innovation Center for Utilization of Botanical Functional Ingredients, Changsha 410128, China

Tea has a lipid-lowering effect through regulating lipid metabolism in different tissues and inhibiting digestion and absorption of lipid. The lipid metabolism pathway affects the synthesis and decomposition of lipid and fat decreasing through regulating the expression of Sterol Regulatory Element Binding Proteins (SREBPs) and its relative factors.

tea, obesity, lipid metabolism, SREBP

TS272；R972+.6

A

1000-369X(2018)01-102-10

2017-06-29

2017-09-20

潘聯(lián)云，女，在讀碩士研究生，主要從事茶葉加工及功能成分化學(xué)研究，jiayoualei@sina.com。*通訊作者： gongyushun@foxmail.com