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提取物可抑制高脂肪饮食诱导肥胖小鼠的肥胖和肝脂肪变性。

Extract Suppresses Obesity and Hepatic Steatosis in High Fat Diet-Induced Obese Mice.

机构信息

Department of Food Science and Biotechnology, College of Life Science, CHA University, Seongnam 13488, Kyeonggi, Korea.

出版信息

Nutrients. 2018 Nov 20;10(11):1802. doi: 10.3390/nu10111802.

DOI:10.3390/nu10111802
PMID:30463291
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6267443/
Abstract

Obesity is caused by the expansion of white adipose tissue (WAT), which stores excess triacylglycerol (TG), this can lead to disorders including type 2 diabetes, atherosclerosis, metabolic diseases. extract (IOE) is prepared from a brown alga and has anti-oxidative properties. We investigated the detailed mechanisms of the anti-obesity activity of IOE. Treatment with IOE blocked lipid accumulation by reducing expression of key adipogenic transcription factors, such as CCAAT/enhancer-binding protein alpha (C/EBPα) and peroxisome proliferator-activated receptor gamma (PPARγ), in 3T3-L1 cells. Administration of IOE to high fat diet (HFD)-fed mice inhibited body and WAT mass gain, attenuated fasting hyperglycemia and dyslipidemia. The obesity suppression was associated with reductions in expression of adipogenic proteins, such as C/EBPα and PPARγ, increases in expression of lipolytic enzymes, such as adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL), in WAT of HFD-fed mice. In addition, IOE-treated mice had lower hepatic TG content, associated with lower protein expression of lipogenic genes, such as diglyceride acyltransferase 1 (DGAT1), sterol regulatory element-binding protein 1 (SREBP1), fatty acid synthase (FAS). IOE treatment also reduced serum free fatty acid concentration, probably through the upregulation of β-oxidation genes, suggested by increases in AMPKα and CPT1 expression in WAT and liver. In summary, IOE ameliorates HFD-induced obesity and its related metabolic disease, hepatic steatosis, by regulating multiple pathways.

摘要

肥胖是由白色脂肪组织 (WAT) 的扩张引起的,其储存过量的三酰基甘油 (TG),这可能导致包括 2 型糖尿病、动脉粥样硬化、代谢疾病等疾病。IOE 是从褐藻中提取的,具有抗氧化特性。我们研究了 IOE 抗肥胖活性的详细机制。IOE 处理通过降低关键脂肪生成转录因子的表达来阻止脂质积累,例如 CCAAT/增强子结合蛋白α (C/EBPα) 和过氧化物酶体增殖物激活受体γ (PPARγ),在 3T3-L1 细胞中。IOE 给药到高脂肪饮食 (HFD) 喂养的小鼠抑制体重和 WAT 质量增加,减轻空腹高血糖和血脂异常。肥胖抑制与脂肪生成蛋白如 C/EBPα 和 PPARγ 的表达降低有关,与 WAT 中的脂肪分解酶如脂肪甘油三酯脂肪酶 (ATGL) 和激素敏感脂肪酶 (HSL) 的表达增加有关在 HFD 喂养的小鼠中。此外,IOE 处理的小鼠肝 TG 含量较低,与脂肪生成基因如二酰基甘油酰基转移酶 1 (DGAT1)、固醇调节元件结合蛋白 1 (SREBP1)、脂肪酸合酶 (FAS) 的蛋白表达降低有关。IOE 处理还降低了血清游离脂肪酸浓度,可能通过增加 WAT 和肝脏中 AMPKα 和 CPT1 的表达来上调 β-氧化基因。总之,IOE 通过调节多种途径改善 HFD 诱导的肥胖及其相关代谢疾病、肝脂肪变性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af06/6267443/a38c878c05b2/nutrients-10-01802-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af06/6267443/8e82937281da/nutrients-10-01802-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af06/6267443/1fdc4e36dff5/nutrients-10-01802-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af06/6267443/11dd999ad935/nutrients-10-01802-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af06/6267443/4feca62aa38a/nutrients-10-01802-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af06/6267443/60b0e2c31bbe/nutrients-10-01802-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af06/6267443/a38c878c05b2/nutrients-10-01802-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af06/6267443/8e82937281da/nutrients-10-01802-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af06/6267443/1fdc4e36dff5/nutrients-10-01802-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af06/6267443/11dd999ad935/nutrients-10-01802-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af06/6267443/4feca62aa38a/nutrients-10-01802-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af06/6267443/60b0e2c31bbe/nutrients-10-01802-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af06/6267443/a38c878c05b2/nutrients-10-01802-g006.jpg

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