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富含精氨酸果糖的济州大麦(L.)提取物对 C57BL/6 小鼠和 3T3-L1 前体脂肪细胞模型的抗肥胖和抗脂肪生成作用。

Anti-Obesity and Anti-Adipogenic Effects of Administration of Arginyl-Fructose-Enriched Jeju Barley ( L.) Extract in C57BL/6 Mice and in 3T3-L1 Preadipocytes Models.

机构信息

Department of Food and Nutrition, Hannam University, Daejeon 34054, Korea.

Institute of Functional Foods, Kunpoong Bio Co., Ltd., Jeju 63010, Korea.

出版信息

Molecules. 2022 May 19;27(10):3248. doi: 10.3390/molecules27103248.

DOI:10.3390/molecules27103248
PMID:35630735
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9143543/
Abstract

In our previous study, we reported that arginyl-fructose (AF), one of the Amadori rearrangement compounds (ARCs) produced by the heat processing of Korean ginseng can reduce carbohydrate absorption by inhibiting intestinal carbohydrate hydrolyzing enzymes in both in vitro and in vivo animal models. This reduced absorption of carbohydrate might be helpful to control body weight gain due to excessive carbohydrate consumption and support induced calorie restriction. However, the weight management effect, except for the effect due to anti-hyperglycemic action, along with the potential mechanism of action have not yet been determined. Therefore, the efforts of this study are to investigate and understand the possible weight management effect and mechanism action of AF-enriched barley extracts (BEE). More specifically, the effect of BEE on lipid accumulation and adipogenic gene expression, body weight gain, body weight, plasma lipids, body fat mass, and lipid deposition were evaluated using C57BL/6 mice and 3T3-L1 preadipocytes models. The formation of lipid droplets in the 3T3-L1 treated with BEE (500 and 750 µg/mL) was significantly blocked (p < 0.05 and p < 0.01, respectively). Male C57BL/6 mice were fed a high-fat diet (30% fat) for 8 weeks with BEE (0.3 g/kg-body weight). Compared to the high fat diet control (HFD) group, the cells treated with BEE significantly decreased in intracellular lipid accumulation with concomitant decreases in the expression of key transcription factors, peroxisome proliferator-activated receptor gamma (PPARγ), CCAAT/enhancer-binding protein alpha (CEBP/α), the mRNA expression of downstream lipogenic target genes such as fatty acid binding protein 4 (FABP4), fatty acid synthase (FAS), and sterol regulatory element-binding protein 1c (SREBP-1c). Supplementation of BEE effectively lowered the body weight gain, visceral fat accumulation, and plasma lipid concentrations. Compared to the HFD group, BEE significantly suppressed body weight gain (16.06 ± 2.44 g vs. 9.40 ± 1.39 g, p < 0.01) and increased serum adiponectin levels, significantly, 1.6-folder higher than the control group. These results indicate that AF-enriched barley extracts may prevent diet-induced weight gain and the anti-obesity effect is mediated in part by inhibiting adipogenesis and increasing adiponectin level.

摘要

在我们之前的研究中,我们报告称,精氨酸果糖(AF)是一种美拉德重排化合物(ARC),由高丽参的热加工产生,可通过抑制体内和体内动物模型的肠道碳水化合物水解酶来减少碳水化合物的吸收。这种减少碳水化合物的吸收可能有助于控制因过度摄入碳水化合物而导致的体重增加,并支持诱导的热量限制。然而,除了抗高血糖作用的作用外,体重管理效果以及潜在的作用机制尚未确定。因此,本研究的努力是研究和了解富含 AF 的大麦提取物(BEE)的可能体重管理效果和作用机制。更具体地说,使用 C57BL/6 小鼠和 3T3-L1 前体脂肪细胞模型评估 BEE 对脂质积累和脂肪生成基因表达、体重增加、体重、血浆脂质、体脂肪质量和脂质沉积的影响。BEE(500 和 750 µg/mL)处理的 3T3-L1 中的脂滴形成明显受阻(分别为 p < 0.05 和 p < 0.01)。雄性 C57BL/6 小鼠用高脂肪饮食(30%脂肪)喂养 8 周,并用 BEE(0.3 g/kg 体重)喂养。与高脂肪饮食对照组(HFD)相比,用 BEE 处理的细胞细胞内脂质积累明显减少,同时关键转录因子过氧化物酶体增殖物激活受体γ(PPARγ)、CCAAT/增强子结合蛋白α(CEBP/α)的表达下降,下游脂肪生成靶基因如脂肪酸结合蛋白 4(FABP4)、脂肪酸合酶(FAS)和固醇调节元件结合蛋白 1c(SREBP-1c)的 mRNA 表达也下降。BEE 的补充有效降低了体重增加、内脏脂肪积累和血浆脂质浓度。与 HFD 组相比,BEE 显著抑制体重增加(16.06 ± 2.44 g 与 9.40 ± 1.39 g,p < 0.01)和显著增加血清脂联素水平,比对照组高 1.6 倍。这些结果表明,富含 AF 的大麦提取物可预防饮食诱导的体重增加,其抗肥胖作用部分通过抑制脂肪生成和增加脂联素水平来介导。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ffd/9143543/62c30b8e4f1d/molecules-27-03248-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ffd/9143543/a2d4a0fdb30a/molecules-27-03248-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ffd/9143543/2147bc83b3dd/molecules-27-03248-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ffd/9143543/bb5d8f9eb7ae/molecules-27-03248-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ffd/9143543/0bbb1612b291/molecules-27-03248-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ffd/9143543/ee5cb899e058/molecules-27-03248-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ffd/9143543/62c30b8e4f1d/molecules-27-03248-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ffd/9143543/a2d4a0fdb30a/molecules-27-03248-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ffd/9143543/2147bc83b3dd/molecules-27-03248-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ffd/9143543/bb5d8f9eb7ae/molecules-27-03248-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ffd/9143543/0bbb1612b291/molecules-27-03248-g004.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ffd/9143543/62c30b8e4f1d/molecules-27-03248-g006.jpg

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