Antiobesity Effect of Flaxseed Polysaccharide via Inducing Satiety due to Leptin Resistance Removal and Promoting Lipid Metabolism through the AMP-Activated Protein Kinase (AMPK) Signaling Pathway
Antiobesity Effect of Flaxseed Polysaccharide via Inducing Satiety due to Leptin Resistance Removal and Promoting Lipid Metabolism through the AMP-Activated Protein Kinase (AMPK) Signaling Pathway
复制标题
亚麻籽多糖通过消除瘦素抗性诱导饱腹感并通过 AMP 激活蛋白激酶 (AMPK) 信号通路促进脂质代谢发挥抗肥胖作用
DOI：
10.1021/acs.jafc.9b02434
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发表时间：
2019-06-26
影响因子：
6.1
通讯作者：
Peng, Xichun
中科院分区：
文献类型：
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作者：
Luo, Jianming;Qi, Jiamei;Peng, Xichun
肥胖是一种世界性的代谢综合征，会导致许多慢性疾病。近年来，我们发现亚麻籽多糖（FP）具有抗肥胖作用，但其作用机制尚不清楚。在这项研究中，大鼠首先被喂食高脂肪食物诱导肥胖。肥胖大鼠分别饲喂对照饲粮AIN-93M （HFD组）和10% FP饲粮（FPD组）。测定并分析了体重、体脂、脂肪组织和肝脏切片、血清总甘油三酯、血清空腹血糖水平、血清胰岛素、血清炎症因子、瘦素-神经肽Y （NPY）和amp活化蛋白激酶（AMPK）信号通路内的血清蛋白。FPD组的体重和腹部脂肪分别从HFD组的530 +/- 16 g和2.15% +/- 0.30%降低到478 +/- 10 g和1.38% +/- 0.48%。这种作用可能是通过抑制炎症和恢复饱腹感来消除瘦素抵抗，其途径是显著下调NPY和上调胰高血糖素样肽1。脂联素可能通过肠-脑轴显著上调，并进一步激活AMPK信号通路，从而改善脂质代谢，包括改善脂肪分解和脂肪酸氧化，抑制脂肪生成。这是关于FP抗肥胖机制的第一篇报道，从而为非淀粉多糖和肥胖提供了一个全面的了解。
Obesity is a metabolic syndrome worldwide that causes many chronic diseases. Recently, we found an antiobesity effect of flaxseed polysaccharide (FP), but the mechanism remains to be elucidated. In this study, rats were first induced to develop obesity by being fed a high-fat diet. The obese rats were then fed a control diet, AIN-93M (group HFD), or a 10% FP diet (group FPD). The body weight, body fat, adipose tissue and liver sections, serous total triglycerides, levels of fasting blood glucose in serum, serous insulin, inflammatory cytokines in serum, and serous proteins within the leptin-neuropeptide Y (NPY) and AMP-activated protein kinase (AMPK) signaling pathway were determined and analyzed. FP intervention significantly reduced body weight and abdominal fat from 530 +/- 16 g and 2.15% +/- 0.30% in group HFD to 478 +/- 10 g and 1.38% +/- 0.48% in group FPD, respectively. This effect was achieved by removing leptin resistance possibly by inhibiting inflammation and recovering satiety through the significant downregulation of NPY and the upregulation of glucagon-like peptide 1. Adiponectin was then significantly upregulated probably via the gut-brain axis and further activated the AMPK signaling pathway to improve lipid metabolism including the improvement of lipolysis and fatty acid oxidation and the suppression of lipogenesis. This is the first report of the proposed antiobesity mechanism of FP, thereby providing a comprehensive understanding of nonstarch polysaccharides and obesity.