Department of Food Science and Engineering , Jinan University , Guangzhou , 510632 Guangdong , China.
College of Life Science and Technology , Jinan University , Guangzhou , 510632 Guangdong , China.
J Agric Food Chem. 2019 Jun 26;67(25):7040-7049. doi: 10.1021/acs.jafc.9b02434. Epub 2019 Jun 14.
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.
肥胖是一种全球性的代谢综合征，可导致许多慢性疾病。最近，我们发现亚麻籽多糖（FP）具有抗肥胖作用，但作用机制尚不清楚。在本研究中，首先用高脂肪饮食喂养大鼠诱导肥胖。然后，肥胖大鼠用对照饮食AIN-93M（HFD 组）或 10%FP 饮食（FPD 组）喂养。测定并分析体重、体脂肪、脂肪组织和肝切片、血清总甘油三酯、空腹血糖水平、血清胰岛素、血清炎症细胞因子以及瘦素-神经肽 Y（NPY）和 AMP 激活蛋白激酶（AMPK）信号通路中的血清蛋白水平。FP 干预可显著降低体重和腹部脂肪，使 HFD 组的体重和腹部脂肪分别从 530±16g 和 2.15%±0.30%降至 FPD 组的 478±10g 和 1.38%±0.48%。这一作用可能是通过抑制炎症和通过显著下调 NPY 和上调胰高血糖素样肽 1 恢复饱腹感来消除瘦素抵抗而实现的。脂联素随后被显著上调，可能是通过肠-脑轴，进一步激活 AMPK 信号通路来改善脂代谢，包括促进脂肪分解和脂肪酸氧化以及抑制脂肪生成。这是 FP 提出的抗肥胖作用机制的首次报道，从而为非淀粉多糖和肥胖提供了全面的认识。
