Department of Food Science and Nutrition, The Catholic University of Korea, Bucheon, Republic of Korea.
Nutr Res. 2019 May;65:54-62. doi: 10.1016/j.nutres.2019.02.002. Epub 2019 Feb 20.
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 μg/mL of fucoidan from Undaria pinnatifida. 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 γ (PPARγ), 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.
岩藻聚糖,一种从褐藻中提取的硫酸化多糖,已被证明可降低小鼠的血糖水平并提高胰岛素敏感性。我们研究了岩藻聚糖对 3T3-L1 细胞中脂质积累、脂肪分解和葡萄糖摄取的影响,以验证岩藻聚糖通过直接作用于脂肪细胞发挥抗糖尿病功能的假说。用从裙带菜中提取的 10、50、100 和 200μg/ml 的岩藻聚糖处理 3T3-L1 细胞。油红 O 染色和 AdipoRed 分析用于测定脂肪细胞分化过程中的脂质积累。岩藻聚糖呈剂量依赖性降低脂质积累和甘油-3-磷酸脱氢酶(GPDH)活性(P<0.01)。过氧化物酶体增殖物激活受体γ(PPARγ)的表达也受到抑制,PPARγ是与脂肪细胞分化相关的主要转录因子。岩藻聚糖处理还刺激正常脂肪细胞的葡萄糖摄取,并恢复肥胖诱导的胰岛素抵抗脂肪细胞的胰岛素刺激的葡萄糖摄取,肥胖诱导的胰岛素抵抗脂肪细胞是通过将肥大的 3T3-L1 细胞与 RAW 264.7 巨噬细胞(RAW-CM)的条件培养基孵育来制备的(P<0.01)。在 RAW-CM 的存在下,岩藻聚糖增强了肾上腺素刺激的脂肪分解,但降低了基础脂肪分解,通过非酯化脂肪酸进入培养基来测定(P<0.001)。这些结果表明,岩藻聚糖可能通过改善胰岛素刺激的葡萄糖摄取和抑制基础脂肪分解而不诱导脂肪生成,从而具有抗糖尿病作用。