内分泌学
内科学
安普克
瘦素
脂联素
胰岛素抵抗
脂质代谢
AMP活化蛋白激酶
脂肪组织
化学
脂肪生成
下调和上调
蛋白激酶A
脂解
胰岛素
生物
激酶
医学
生物化学
肥胖
基因
作者
Jianming Luo,Jiamei Qi,Wenjun Wang,Zhenhuan Luo,Liu Liu,Guangwen Zhang,Qinghua Zhou,Jiesheng Liu,Xichun Peng
标识
DOI:10.1021/acs.jafc.9b02434
摘要
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.
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