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首页> 外文期刊>Nutrition Research >Fucoidan from Undaria pinnatifida has anti-diabetic effects by stimulation of glucose uptake and reduction of basal lipolysis in 3T3-L1 adipocytes
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Fucoidan from Undaria pinnatifida has anti-diabetic effects by stimulation of glucose uptake and reduction of basal lipolysis in 3T3-L1 adipocytes

机译:来自甲状腺葡萄糖的Fucoinean通过刺激葡萄糖吸收和减少3T3-L1 adipocytes的基础脂肪分解具有抗糖尿病效应

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摘要

Fucoidan, a sulfated polysaccharide derived from brown seaweeds, has been shown to reduce blood glucose levels and improve insulin sensitivity in mice. We investigated the effects of fucoidan on lipid accumulation, lipolysis, and glucose uptake in 3T3-L1 cells to test the hypothesis that fucoidan exerts an anti-diabetic function by acting directly on adipocytes. The 3T3-L1 cells were treated with 10, 50, 100, and 200 mu g/mL of fucoidan from Undaria pinnatflda. Oil Red O staining and AdipoRed assay were used to determine lipid accumulation during adipocyte differentiation. Fucoidan was shown to reduce lipid accumulation and glycerol-3-phosphate dehydrogenase (GPDH) activity in a dose-dependent manner (P .01). The expression of peroxisome proliferator-activated receptor gamma (PPAR gamma), a major transcription factor associated with adipocyte differentiation, was also suppressed upon treatment with fucoidan. Treatment with fucoidan stimulated glucose uptake in normal adipocytes and restored insulin-stimulated glucose uptake in obesity-induced insulin resistant adipocytes, which were made by incubating hypertrophied 3T3-L1 cells with the conditioned media of RAW 264.7 macrophages (RAW-CM) (P .01). In the presence of RAW-CM, fucoidan enhanced epinephrine-stimulated lipolysis but reduced basal lipolysis, as determined by non-esterified fatty acid into the culture medium (P .001). These results suggest that fucoidan may have anti-diabetic effects by improving insulin-stimulated glucose uptake and inhibiting basal lipolysis in adipocytes without inducing adipogenesis. (C) 2019 Elsevier Inc. All rights reserved.
机译:硫磺酸,衍生自棕色海藻的硫酸化多糖,已被证明降低血糖水平并提高小鼠胰岛素敏感性。我们调查了岩藻糖糖对3T3-L1细胞脂质积累,脂解和葡萄糖摄取的影响,以测试FUCOINON通过直接作用于脂肪细胞的抗糖尿病功能的假设。用10,50,100和200μmg/ ml从甲状腺内脏的uCucoinoN处理3T3-L1细胞。油红色O染色和探讨测定用于确定脂肪细胞分化期间的脂质积累。显示岩藻酮以剂量依赖性方式减少脂质积累和甘油-3-磷酸脱氢酶(GPDH)活性(P <.01)。在用岩藻糖烷处理时,还抑制了过氧化物酶促增殖物激活受体γ(PPARγ),与脂肪细胞分化相关的主要转录因子。用岩藻糖糖刺激葡萄糖摄取在正常的脂肪细胞中并恢复肥胖诱导的胰岛素抗性脂肪细胞中的胰岛素刺激的葡萄糖摄取,其通过将肥大3T3-L1细胞与原料264.7巨噬细胞(RAW-CM)的条件培养基培养(P&Lt。 ; 01)。在原始CM的存在下,岩藻糖蛋白增强的肾上腺素刺激的脂解,但基础脂肪分解的降低,如非酯化脂肪酸所测定到培养基中(P <.001)。这些结果表明,通过改善胰岛素刺激的葡萄糖摄取和抑制脂肪细胞的基础脂肪解性而不诱导脂肪发生,抗糖尿病可能具有抗糖尿病作用。 (c)2019 Elsevier Inc.保留所有权利。

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