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小花山柰根茎提取物对高脂饮食诱导的肥胖C57BL/6N小鼠具有抗肥胖作用。

Kaempferia parviflora rhizome extract exerts anti-obesity effect in high-fat diet-induced obese C57BL/6N mice.

作者信息

Lee Hyun Sook, Jeon Young Eun, Awa Riyo, Yoshino Susumu, Kim Eun Ji

机构信息

Department of Food Science & Nutrition, Dongseo University, Busan, Korea.

Industry Coupled Cooperation Center for Bio Healthcare Materials, Hallym University, Chuncheon, Korea.

出版信息

Food Nutr Res. 2023 Aug 23;67. doi: 10.29219/fnr.v67.9413. eCollection 2023.

DOI:10.29219/fnr.v67.9413
PMID:37691744
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10492229/
Abstract

(KP) rhizome, also called black ginger, has been used as a herbal medicine for many centuries. This current study was aimed at exploring whether KP rhizome extract (KPE) had anti-obesity effects and the mechanism involved. Five-week-old C57BL/6N male mice were allocated into five groups for 8-week feeding with control diet (CD), high-fat diet (HFD), HFD + 150 mg/kg body weight (BW)/day KPE (HFD+K150), HFD + 300 mg/kg BW/day KPE (HFD+K300), and HFD + 600 mg/kg BW/day KPE (HFD+K600). KPE decreased BW, body fat mass, adipose tissue weight, adipocyte size, and serum levels of glucose, triglycerides, cholesterol, insulin, and leptin in HFD-induced obese C57BL/6N mice. KPE inhibited adipogenesis by decreasing CCAAT/enhancer binding protein α, peroxisome proliferator-activated receptor γ, sterol regulatory element-binding protein-1c, acetyl-CoA carboxylase 1, ATP-citrate lyase, and fatty acid synthase mRNA expression. KPE improved lipolysis by increasing carnitine palmitoyl transferase 1 and hormone-sensitive lipase mRNA expression. These results suggest that KPE may have inhibited HFD-induced obesity by regulating several pathways involved in decreasing adipogenesis and enhancing lipolysis. Thus, the results suggest that KPE (or KP) may be applicable as an anti-obesity agent.

摘要

(KP) 根茎,也称为黑姜,几个世纪以来一直被用作草药。本研究旨在探讨KP根茎提取物 (KPE) 是否具有抗肥胖作用及其相关机制。将5周龄的C57BL/6N雄性小鼠分为五组,分别用对照饮食 (CD)、高脂饮食 (HFD)、HFD + 150 mg/kg体重 (BW)/天KPE (HFD+K150)、HFD + 300 mg/kg BW/天KPE (HFD+K300) 和HFD + 600 mg/kg BW/天KPE (HFD+K600) 喂养8周。KPE可降低高脂饮食诱导的肥胖C57BL/6N小鼠的体重、体脂肪量、脂肪组织重量、脂肪细胞大小以及血糖、甘油三酯、胆固醇、胰岛素和瘦素的血清水平。KPE通过降低CCAAT/增强子结合蛋白α、过氧化物酶体增殖物激活受体γ、固醇调节元件结合蛋白-1c、乙酰辅酶A羧化酶1、ATP-柠檬酸裂解酶和脂肪酸合酶的mRNA表达来抑制脂肪生成。KPE通过增加肉碱棕榈酰转移酶1和激素敏感性脂肪酶的mRNA表达来改善脂肪分解。这些结果表明,KPE可能通过调节参与减少脂肪生成和增强脂肪分解的多种途径来抑制高脂饮食诱导的肥胖。因此,结果表明KPE (或KP) 可能作为一种抗肥胖剂适用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a10/10492229/c71632283636/FNR-67-9413-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a10/10492229/031e9860e1ea/FNR-67-9413-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a10/10492229/714b9dfc215f/FNR-67-9413-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a10/10492229/b637527ef502/FNR-67-9413-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a10/10492229/de330e83874f/FNR-67-9413-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a10/10492229/c71632283636/FNR-67-9413-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a10/10492229/031e9860e1ea/FNR-67-9413-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a10/10492229/714b9dfc215f/FNR-67-9413-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a10/10492229/b637527ef502/FNR-67-9413-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a10/10492229/de330e83874f/FNR-67-9413-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a10/10492229/c71632283636/FNR-67-9413-g005.jpg

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