浒苔硫酸化多糖通过依赖AMP活化蛋白激酶的途径减轻高脂饮食诱导肥胖小鼠的脂质代谢紊乱。
Sulfated Polysaccharides from Enteromorpha prolifera Attenuate Lipid Metabolism Disorders in Mice with Obesity Induced by a High-Fat Diet via a Pathway Dependent on AMP-Activated Protein Kinase.
作者信息
Zhao Aili, Chen Yiqin, Li Yixin, Lin Dai, Yang Zheng, Wang Qi, Chen Hui, Xu Qian, Chen Jie, Zhu Pingping, Huang Fang, Huang Zuxiong, Ren Rendong, Lin Wenting, Wang Wenxiang
机构信息
Fujian Province Key Laboratory of Environment and Health, School of Public Health, Fujian Medical University, Fuzhou, Fujian Province, China; Department of Health Inspection and Quarantine, School of Public Health, Fujian Medical University, Fuzhou, Fujian Province, China; Department of Nutrition and Food Safety, School of Public Health, Fujian Medical University, Fuzhou, Fujian Province, China.
Fujian Province Key Laboratory of Environment and Health, School of Public Health, Fujian Medical University, Fuzhou, Fujian Province, China; Department of Health Inspection and Quarantine, School of Public Health, Fujian Medical University, Fuzhou, Fujian Province, China.
出版信息
J Nutr. 2022 Apr;152(4):939-949. doi: 10.1093/jn/nxab432. Epub 2023 Feb 18.
BACKGROUND
Obesity-related metabolic diseases have recently evoked worldwide attention. Studies have demonstrated that Enteromorpha polysaccharide (EP) exerts lipid-lowering effects, but the underlying mechanism remains unclear.
OBJECTIVES
We investigated whether EP regulates lipid metabolism disorders in mice with high-fat diet (HFD)-induced obesity via an AMP-activated protein kinase (AMPK)-dependent pathway.
METHODS
Six-week-old male C57BL/6J mice (18 ± 2 g) were fed a normal diet (ND; 10% energy from fats) or an HFD (60% energy from fats) for 6 weeks to induce obesity and treated intragastrically with EP (200 mg/kg body weight) or distilled water (10 mL/kg body weight) for 8 weeks. Biochemical indicators, AMPK-dependent pathways, and lipid metabolism-related genes were evaluated to assess the effects of EP on HFD-induced lipid metabolism disorders. The essential role of AMPK in the EP-mediated regulation of lipid metabolism was confirmed using HFD-fed male Ampka2-knockout mice (aged 6 weeks; 17 ± 2 g) treated or not treated with the above-mentioned dose of EP. The data were analyzed by t-tests, 2-factor and 1-way ANOVAs.
RESULTS
Compared to the ND, the HFD resulted in a greater body weight (24.3%), perirenal fat index (2.2-fold), and serum total cholesterol (24.66%) and LDL cholesterol (1.25-fold) concentrations (P < 0.05) and dysregulated the AMPK-dependent pathway and the expression of most lipid metabolism-related genes (P < 0.05). Compared to the HFD, EP treatment resulted in a lower perirenal fat index (31.22%) and LDL cholesterol concentration (23.98%) and partly reversed the dysregulation of the AMPK-dependent pathway and the altered expression of lipid metabolism-related genes (P < 0.05). Ampka2 knockout abolished the above-mentioned effects of EP in obese mice and the EP-mediated effects on the expression of lipid metabolism-related genes (P > 0.05).
CONCLUSIONS
These findings suggest that EP can ameliorate lipid metabolism disorders in mice with HFD-induced obesity via an AMPK-dependent pathway.
背景
肥胖相关的代谢性疾病近来引起了全球关注。研究表明浒苔多糖（EP）具有降脂作用，但其潜在机制仍不清楚。
目的
我们研究了EP是否通过AMP激活的蛋白激酶（AMPK）依赖性途径调节高脂饮食（HFD）诱导的肥胖小鼠的脂质代谢紊乱。
方法
6周龄雄性C57BL/6J小鼠（18±2 g）分别给予正常饮食（ND；10%能量来自脂肪）或HFD（60%能量来自脂肪）6周以诱导肥胖，然后分别用EP（200 mg/kg体重）或蒸馏水（10 mL/kg体重）灌胃8周。评估生化指标、AMPK依赖性途径和脂质代谢相关基因，以评价EP对HFD诱导的脂质代谢紊乱的影响。使用给予HFD的雄性Ampka2基因敲除小鼠（6周龄；17±2 g），给予或不给予上述剂量的EP，以证实AMPK在EP介导的脂质代谢调节中的重要作用。数据采用t检验、双因素和单因素方差分析进行分析。
结果
与ND组相比，HFD组小鼠体重增加（24.3%）、肾周脂肪指数增加（2.2倍）、血清总胆固醇浓度增加（24.66%）和低密度脂蛋白胆固醇浓度增加（1.25倍）（P<0.05），且AMPK依赖性途径及大多数脂质代谢相关基因的表达失调（P<0.05）。与HFD组相比，EP治疗组肾周脂肪指数降低（31.22%），低密度脂蛋白胆固醇浓度降低（23.98%），部分逆转了AMPK依赖性途径的失调及脂质代谢相关基因表达的改变（P<0.05）。Ampka2基因敲除消除了EP对肥胖小鼠的上述作用以及EP对脂质代谢相关基因表达的介导作用（P>0.05）。
结论
这些发现表明，EP可通过AMPK依赖性途径改善HFD诱导的肥胖小鼠的脂质代谢紊乱。
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