Anti-Obesity and Anti-Adipogenic Effects of Chitosan Oligosaccharide (GO2KA1) in SD Rats and in 3T3-L1 Preadipocytes Models.
Anti-Obesity and Anti-Adipogenic Effects of Chitosan Oligosaccharide (GO2KA1) in SD Rats and in 3T3-L1 Preadipocytes Models.
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DOI：
10.3390/molecules26020331
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发表时间：
2021-01-11
期刊：
影响因子：
--
通讯作者：
Kwon YI
中科院分区：
文献类型：
--
作者：
Lee JY;Kim TY;Kang H;Oh J;Park JW;Kim SC;Kim M;Apostolidis E;Kim YC;Kwon YI
体重过重是2型糖尿病（T2 D）和相关代谢并发症的主要风险因素，体重减轻已被证明可改善T2 D患者的血糖控制并降低发病率和死亡率。采用饮食干预的减肥策略可显著降低糖尿病相关代谢紊乱。我们以前曾报道，补充低分子壳寡糖（GO2 KA 1）显着抑制动物和人类的血糖水平。然而，GO2 KA 1对肥胖的影响仍然不清楚。本研究的目的是使用3 T3-L1脂肪细胞在体外评价GO2 KA 1对脂质蓄积和成脂基因表达的抗肥胖作用，并使用Sprague-Dawley（SD）大鼠模型评价血浆脂质谱。在存在和不存在不同浓度的GO2 KA 1的情况下，在脂肪形成刺激下刺激小鼠3 T3-L1前脂肪细胞分化。通过脂质油红O染色和成脂基因表达证实脂肪细胞分化。与对照组相比，GO2 KA 1处理的细胞内脂质积聚显著减少，同时关键转录因子过氧化物酶体增殖物激活受体γ（PPARγ）和CCAAT/增强子结合蛋白α（CEBP/α）的表达降低。与对照组相比，GO2 KA 1处理组脂肪酸结合蛋白4（FABP 4）、脂肪酸合成酶（FAS）等下游成脂靶基因的mRNA表达明显降低。在体内，给雄性SD大鼠喂食高脂饮食（HFD）6周以诱导肥胖，随后口服给予0.1 g/kg/体重的GO2 KA 1或HFD中的载体对照。我们评估了体重、食物摄入量、血脂、肝功能的丙氨酸氨基转移酶（ALT）和天冬氨酸氨基转移酶（AST）水平以及肥胖介导的代谢综合征的标志物脂联素的血清水平。与对照组相比，GO2 KA 1显著抑制体重增加（185.8 ± 8.8 g对211.6 ± 20.1 g，p < 0.05），在食物摄入方面无显著差异。GO2 KA 1治疗组的血清总胆固醇、甘油三酯和低密度脂蛋白（LDL）水平显著低于对照组，而GO2 KA 1组的高密度脂蛋白（HDL）水平高于对照组。与对照组相比，GO2 KA 1治疗组还显示ALT和AST水平显著降低。此外，血清脂联素水平显著高于对照组1.5倍。这些体内和体外研究结果表明，饮食中补充GO2 KA 1可以防止饮食诱导的体重增加，抗肥胖作用部分是通过抑制脂肪形成和增加脂联素水平介导的。
Excess body weight is a major risk factor for type 2 diabetes (T2D) and associated metabolic complications, and weight loss has been shown to improve glycemic control and decrease morbidity and mortality in T2D patients. Weight-loss strategies using dietary interventions produce a significant decrease in diabetes-related metabolic disturbance. We have previously reported that the supplementation of low molecular chitosan oligosaccharide (GO2KA1) significantly inhibited blood glucose levels in both animals and humans. However, the effect of GO2KA1 on obesity still remains unclear. The aim of the study was to evaluate the anti-obesity effect of GO2KA1 on lipid accumulation and adipogenic gene expression using 3T3-L1 adipocytes in vitro and plasma lipid profiles using a Sprague-Dawley (SD) rat model. Murine 3T3-L1 preadipocytes were stimulated to differentiate under the adipogenic stimulation in the presence and absence of varying concentrations of GO2KA1. Adipocyte differentiation was confirmed by Oil Red O staining of lipids and the expression of adipogenic gene expression. Compared to control group, the cells treated with GO2KA1 significantly decreased in intracellular lipid accumulation with concomitant decreases in the expression of key transcription factors, peroxisome proliferator-activated receptor gamma (PPARγ) and CCAAT/enhancer-binding protein alpha (CEBP/α). Consistently, the mRNA expression of downstream adipogenic target genes such as fatty acid binding protein 4 (FABP4), fatty acid synthase (FAS), were significantly lower in the GO2KA1-treated group than in the control group. In vivo, male SD rats were fed a high fat diet (HFD) for 6 weeks to induced obesity, followed by oral administration of GO2KA1 at 0.1 g/kg/body weight or vehicle control in HFD. We assessed body weight, food intake, plasma lipids, levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) for liver function, and serum level of adiponectin, a marker for obesity-mediated metabolic syndrome. Compared to control group GO2KA1 significantly suppressed body weight gain (185.8 ± 8.8 g vs. 211.6 ± 20.1 g, p < 0.05) with no significant difference in food intake. The serum total cholesterol, triglyceride, and low-density lipoprotein (LDL) levels were significantly lower in the GO2KA1-treated group than in the control group, whereas the high-density lipoprotein (HDL) level was higher in the GO2KA1 group. The GO2KA1-treated group also showed a significant reduction in ALT and AST levels compared to the control. Moreover, serum adiponectin levels were significantly 1.5-folder higher than the control group. These in vivo and in vitro findings suggest that dietary supplementation of GO2KA1 may prevent diet-induced weight gain and the anti-obesity effect is mediated in part by inhibiting adipogenesis and increasing adiponectin level.
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影响因子：
3.7
作者：
Chu SH;Lee MK;Ahn KY;Im JA;Park MS;Lee DC;Jeon JY;Lee JW
通讯作者：
Lee JW
DOI：
10.1002/oby.20671
发表时间：
2014-04
期刊：
Obesity (Silver Spring, Md.)
影响因子：
--
作者：
Gawronska-Kozak B;Staszkiewicz J;Gimble JM;Kirk-Ballard H
通讯作者：
Kirk-Ballard H
影响因子：
--
作者：
Kim JG;Jo SH;Ha KS;Kim SC;Kim YC;Apostolidis E;Kwon YI
通讯作者：
Kwon YI
影响因子：
2.9
作者：
Jo, Sung-Hoon;Ha, Kyoung-Soo;Kwon, Young-In
通讯作者：
Kwon, Young-In
影响因子：
5.9
作者：
Klop B;Elte JW;Cabezas MC
通讯作者：
Cabezas MC