Kudo Maya, Gao Ming, Hayashi Misa, Kobayashi Yukiko, Yang Jinwei, Liu Tonghua
School of Pharmacy and Pharmaceutical Science, Mukogawa Women's University, Nishinomiya, Hyogo, Japan.
Institute for Bioscience, Mukogawa Women's University, Nishinomiya, Hyogo, Japan.
Food Nutr Res. 2024 Jan 22;68. doi: 10.29219/fnr.v68.10307. eCollection 2024.
Obesity is closely associated with several chronic diseases, and adipose tissue plays a major role in modulating energy metabolism.
This study aimed to determine whether Mate, derived from A.St.-Hil., ameliorates lipid metabolism in 3T3-L1 adipocytes and high-fat diet (HFD)-fed obese Sprague-Dawley (SD) rats.
3T3-L1 adipocytes were cultured for 7 days, following which intracellular lipid accumulation and expression levels of lipid metabolism-related factors were examined. Dorsomorphin was used to investigate the potential pathways involved, particularly the adenosine monophosphate-activated protein kinase (AMPK)- dependent pathway. Mate was administered to rat HFD-fed obese SD models for 8 consecutive weeks. The expression of lipid metabolism-related factors in the organs and tissues collected from dissected SD rats was evaluated.
Mate suppressed intracellular lipid accumulation in 3T3-L1 adipocytes, increased the protein and gene expression levels of AMPK, hormone sensitive lipase (HSL), calmodulin kinase kinase (CaMKK), liver kinase B1 (LKB1), protein kinase A (PKA), CCAAT/enhancer binding protein (C/EBP), insulin receptor b (IR), and insulin receptor substrate 1 (IRS1) (Tyr465), and decreased those of sterol regulatory element binding protein 1C (), fatty acid synthase (FAS), peroxisome-activated receptor γ (PPARγ), and IRS1 (Ser1101). Furthermore, an AMPK inhibitor abolished the effects exerted by Mate on intracellular lipid accumulation and HSL and FAS expression levels. Mate treatment suppressed body weight gain and improved serum cholesterol levels in HFD-fed obese SD rats. Treatment with Mate increased the protein and gene expression levels of AMPK, PKA, Erk1/Erk2 (p44/p42), and uncoupling protein 1 and reduced those of mammalian target of rapamycin, S6 kinase, , FAS, , and in rat HFD-fed obese SD models.
Mate suppressed intracellular lipid accumulation in 3T3-L1 adipocytes and improved lipid metabolism in the epididymal adipose tissue of HFD-fed obese SD rats via the activation of AMPK-dependent and insulin signaling pathways.
肥胖与多种慢性疾病密切相关，脂肪组织在调节能量代谢中起主要作用。
本研究旨在确定源自圣伊莱尔的马黛茶是否能改善3T3-L1脂肪细胞和高脂饮食（HFD）喂养的肥胖Sprague-Dawley（SD）大鼠的脂质代谢。
将3T3-L1脂肪细胞培养7天，之后检测细胞内脂质积累及脂质代谢相关因子的表达水平。使用多索茶碱研究潜在的相关途径，特别是腺苷单磷酸激活的蛋白激酶（AMPK）依赖性途径。将马黛茶连续8周给予HFD喂养的肥胖SD大鼠模型。评估从解剖的SD大鼠收集的器官和组织中脂质代谢相关因子的表达。
马黛茶抑制3T3-L1脂肪细胞内的脂质积累，增加AMPK、激素敏感性脂肪酶（HSL）、钙调蛋白激酶激酶（CaMKK）、肝激酶B1（LKB1）、蛋白激酶A（PKA）、CCAAT/增强子结合蛋白（C/EBP）、胰岛素受体b（IR）和胰岛素受体底物1（IRS1）（Tyr465）的蛋白和基因表达水平，并降低固醇调节元件结合蛋白1C、脂肪酸合酶（FAS）、过氧化物酶体激活受体γ（PPARγ）和IRS1（Ser1101）的表达水平。此外，AMPK抑制剂消除了马黛茶对细胞内脂质积累以及HSL和FAS表达水平的影响。马黛茶治疗抑制HFD喂养的肥胖SD大鼠的体重增加并改善血清胆固醇水平。在HFD喂养的肥胖SD大鼠模型中，马黛茶治疗增加了AMPK、PKA、细胞外信号调节激酶1/细胞外信号调节激酶2（p44/p42）和解偶联蛋白1的蛋白和基因表达水平，并降低了雷帕霉素靶蛋白、S6激酶、FAS、和的表达水平。
马黛茶通过激活AMPK依赖性和胰岛素信号通路抑制3T3-L1脂肪细胞内的脂质积累，并改善HFD喂养的肥胖SD大鼠附睾脂肪组织中的脂质代谢。
