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Porelis是一种标准化的紫茶提取物,通过调节高脂饮食诱导的C57BL/6小鼠的瘦素和脂联素水平来改善脂肪细胞功能。

Porelis, a standardized purple tea extract, improves adipocyte functionality by regulating the leptin and adiponectin levels in high-fat diet-induced C57BL/6 mice.

作者信息

Sudeep Heggar Venkataramana, Sundeep Kuppam, Venkatakrishna Karempudi, Raj Amrutha, Bhumika Ranganath, Prasanna Kumar Thammatadhahalli Parameshwarappa, Shyamprasad Kodimule

机构信息

R&D Center for Excellence, Vidya Herbs Pvt Ltd., #14A, Jigani I phase, Bangalore- 560 105, Karnataka, India.

出版信息

Iran J Basic Med Sci. 2025;28(8):1037-1046. doi: 10.22038/ijbms.2025.84192.18209.

DOI:10.22038/ijbms.2025.84192.18209
PMID:40584451
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12203826/
Abstract

OBJECTIVES

Purple tea variety of (L.) Kuntze (Theaceae), with its unique presence of anthocyanins and 1,2-di--galloyl-4,6--(S)-hexahydroxydiphenoyl-β-D-glucose (GHG), has enormous potential in the weight management. Here, the weight loss mechanism of a standardized purple tea hydroalcoholic extract (Porelis, 3-5% GHG) is demonstrated in high-fat-diet-induced mice.

MATERIALS AND METHODS

Male C57BL/6 mice (20±2 g) were divided into five groups (n=8). In a 12-week study, the control group was given a normal diet, and the other groups were given HFD (60 % kcal from fat) for 12 weeks. The treatment groups received Porelis at 25, 50, and 100 mg/kg body weight, PO.

RESULTS

Porelis treatment markedly reduced the body weight, fat pad weights, hepatic lipid accumulation, and oxidative stress in the HFD mice. The adipogenic markers, CCAAT/enhancer binding protein alpha (C/EBPα), Peroxisome proliferator-activated receptor gamma (PPAR-γ), and Sterol Regulatory Element Binding Protein 1 (SREBP1) were down-regulated in Porelis-treated mice compared to HFD model group (<0.0001). Porelis treatment reduced the serum leptin level (<0.0001) while increasing the adiponectin (<0.01) in HFD mice. The circulating trimethylamine N-oxide (TMAO) (<0.0001) and insulin (<0.001) levels were significantly reduced in the Porelis groups compared to the HFD-alone group. In addition, Porelis markedly inhibited the pancreatic lipase activity (IC = 223.3 µg/ml).

CONCLUSION

Porelis exerts antiobesity activity in mice by regulating adipogenesis and energy homeostasis. Our data encourages further validation of Porelis-mediated weight loss effects in human subjects.

摘要

目的

山茶科山茶属的紫茶品种,因其独特的花青素和1,2 - 二 - 没食子酰基 - 4,6 - (S) - 六羟基二苯甲酰基 - β - D - 葡萄糖(GHG)成分,在体重管理方面具有巨大潜力。在此,我们展示了标准化紫茶水醇提取物(Porelis,含3 - 5% GHG)对高脂饮食诱导小鼠的减肥机制。

材料与方法

雄性C57BL / 6小鼠(20±2 g)分为五组(n = 8)。在为期12周的研究中,对照组给予正常饮食,其他组给予高脂饮食(60%千卡热量来自脂肪)12周。治疗组经口给予体重25、50和100 mg / kg的Porelis。

结果

Porelis治疗显著降低了高脂饮食小鼠的体重、脂肪垫重量、肝脏脂质积累和氧化应激。与高脂饮食模型组相比,Porelis治疗的小鼠中脂肪生成标志物CCAAT / 增强子结合蛋白α(C / EBPα)、过氧化物酶体增殖物激活受体γ(PPAR - γ)和甾醇调节元件结合蛋白1(SREBP1)下调(<0.0001)。Porelis治疗降低了高脂饮食小鼠的血清瘦素水平(<0.0001),同时增加了脂联素水平(<0.01)。与仅给予高脂饮食的组相比,Porelis组的循环三甲胺N - 氧化物(TMAO)(<0.0001)和胰岛素(<0.001)水平显著降低。此外,Porelis显著抑制了胰脂肪酶活性(IC50 = 223.3 µg / ml)。

结论

Porelis通过调节脂肪生成和能量稳态在小鼠中发挥抗肥胖活性。我们的数据鼓励进一步验证Porelis对人类受试者的减肥效果。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec08/12203826/c32f6cc98922/ijbms-28-1037-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec08/12203826/2ec04ea6c6bb/ijbms-28-1037-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec08/12203826/a1be552f64ce/ijbms-28-1037-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec08/12203826/bfaa485ed83e/ijbms-28-1037-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec08/12203826/22f81767b9b0/ijbms-28-1037-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec08/12203826/2814980a70d8/ijbms-28-1037-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec08/12203826/451f83948351/ijbms-28-1037-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec08/12203826/772162451b89/ijbms-28-1037-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec08/12203826/f424a8df022f/ijbms-28-1037-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec08/12203826/c32f6cc98922/ijbms-28-1037-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec08/12203826/2ec04ea6c6bb/ijbms-28-1037-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec08/12203826/a1be552f64ce/ijbms-28-1037-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec08/12203826/bfaa485ed83e/ijbms-28-1037-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec08/12203826/22f81767b9b0/ijbms-28-1037-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec08/12203826/2814980a70d8/ijbms-28-1037-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec08/12203826/451f83948351/ijbms-28-1037-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec08/12203826/772162451b89/ijbms-28-1037-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec08/12203826/f424a8df022f/ijbms-28-1037-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec08/12203826/c32f6cc98922/ijbms-28-1037-g009.jpg

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