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海洋褐藻岩藻聚糖硫酸酯抑制脂质积累。

Fucoidan from Marine Brown Algae Inhibits Lipid Accumulation.

机构信息

Radiation Biotechnology Research Division, Advanced Radiation Technology Institute (ARTI), Korea Atomic Energy Research Institute (KAERI), 1266 Shinjeong-dong, Jeongeup-si, Jeollabuk-do 580-185, Korea.

出版信息

Mar Drugs. 2011;9(8):1359-1367. doi: 10.3390/md9081359. Epub 2011 Aug 10.

DOI:10.3390/md9081359
PMID:21892350
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3164378/
Abstract

In this study, we elucidated the inhibitory effect of fucoidan from marine brown algae on the lipid accumulation in differentiated 3T3-L1 adipocytes and its mechanism. The treatment of fucoidan in a dose-dependent manner was examined on lipid inhibition in 3T3-L1 cells by using Oil Red O staining. Fucoidan showed high lipid inhibition activity at 200 μg/mL concentration (P < 0.001). Lipolytic activity in adipocytes is highly dependent on hormone sensitive lipase (HSL), which is one of the most important targets of lipolytic regulation. Here, we examined the biological response of fucoidan on the protein level of lipolysis pathway. The expressed protein levels of total hormone sensitive lipase (HSL) and its activated form, phosphorylated-HSL were significantly increased at concentration of 200 μg/mL fucoidan. Furthermore, insulin-induced 2-deoxy-D-[³H] glucose uptake was decreased up to 51% in fucoidan-treated cells as compared to control. Since increase of HSL and p-HSL expression and decrease of glucose uptake into adipocytes are known to lead to stimulation of lipolysis, our results suggest that fucoidan reduces lipid accumulation by stimulating lipolysis. Therefore, these results suggest that fucoidan can be useful for the prevention or treatment of obesity due to its stimulatory lipolysis.

摘要

在这项研究中,我们阐明了海洋褐藻岩藻聚糖对分化的 3T3-L1 脂肪细胞中脂质积累的抑制作用及其机制。通过油红 O 染色,以剂量依赖的方式检查岩藻聚糖对 3T3-L1 细胞中脂质抑制的作用。岩藻聚糖在 200μg/mL 浓度下表现出很高的脂质抑制活性(P<0.001)。脂肪细胞中的脂肪分解活性高度依赖于激素敏感脂肪酶(HSL),它是脂肪分解调节的最重要靶标之一。在这里,我们研究了岩藻聚糖对脂肪分解途径蛋白水平的生物学反应。在 200μg/mL 岩藻聚糖浓度下,总激素敏感脂肪酶(HSL)及其激活形式磷酸化-HSL 的表达蛋白水平显著增加。此外,与对照组相比,岩藻聚糖处理的细胞中胰岛素诱导的 2-脱氧-D-[³H]葡萄糖摄取减少了多达 51%。由于 HSL 和 p-HSL 表达的增加以及葡萄糖向脂肪细胞内摄取的减少已知会导致脂肪分解的刺激,我们的结果表明岩藻聚糖通过刺激脂肪分解来减少脂质积累。因此,这些结果表明岩藻聚糖可通过刺激脂肪分解而用于预防或治疗肥胖症。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9e3/3164378/e66b74d94a66/marinedrugs-09-01359f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9e3/3164378/10f75a4066a8/marinedrugs-09-01359f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9e3/3164378/3b66a6afd3ce/marinedrugs-09-01359f2a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9e3/3164378/0cc10088d0ad/marinedrugs-09-01359f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9e3/3164378/623336983a78/marinedrugs-09-01359f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9e3/3164378/e66b74d94a66/marinedrugs-09-01359f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9e3/3164378/10f75a4066a8/marinedrugs-09-01359f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9e3/3164378/3b66a6afd3ce/marinedrugs-09-01359f2a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9e3/3164378/0cc10088d0ad/marinedrugs-09-01359f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9e3/3164378/623336983a78/marinedrugs-09-01359f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9e3/3164378/e66b74d94a66/marinedrugs-09-01359f5.jpg

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