Key Laboratory for Space Bioscience and Biotechnology, School of Life Sciences, Northwestern Polytechnical University, Xi'an 710072, Shaanxi, People's Republic of China.
College of Food Engineering and Nutritional Science, Shaanxi Normal University, Xi'an 710119, Shaanxi, People's Republic of China.
Int J Biol Macromol. 2021 Jul 1;182:825-837. doi: 10.1016/j.ijbiomac.2021.04.070. Epub 2021 Apr 14.
Artemisia sphaerocephala Krasch polysaccharide (ASKP) consists of two main fractions, 60P (molecular weight at 551 kDa) and 60S (molecular weight at 39 kDa). The anti-obesity effects of ASKP and its two fractions were investigated in high-fat-diet-fed mice and showed similar capability in efficiently preventing the development of obesity. The final body weight and body weight gain of obesity mice model were reduced by 12.44% and 35.33% by ASKP, 10.63% and 34.35% by 60P, and 7.82% and 20.04% by 60S. They also showed similar efficiency to ameliorate dyslipidemia, systematic inflammation, and gut dysbiosis. The colonic genes of barrier integrity were significantly upregulated and the genes of hepatic lipid metabolism and that of colonic inflammatory response were suppressed. They attenuated the gut dysbiosis in obese mice, such as the significant enrichment of beneficial genera (Bifidobacterium and Olsenella) and suppression of harmful ones (Mucispirillum and Helicobacter). Significant enrichment of carbohydrate metabolism associated with the promotion of short-chain fatty acid production and decrease of the metabolisms related to obesity and gut dysbiosis (valine, leucine, and isoleucine biosynthesis, and nitrogen metabolism) were also observed by the administration of ASKP, 60P, and 60S. Overall, these polysaccharides showed potential in acting as prebiotics in preventing high-fat-diet-induced obesity.
球菊苣多糖（ASKP）由两个主要部分组成，60P（分子量为 551 kDa）和 60S（分子量为 39 kDa）。在高脂肪饮食喂养的小鼠中研究了 ASKP 及其两个部分的抗肥胖作用，结果表明它们具有相似的有效预防肥胖发展的能力。肥胖小鼠模型的最终体重和体重增加分别被 ASKP 降低了 12.44%和 35.33%，60P 降低了 10.63%和 34.35%，60S 降低了 7.82%和 20.04%。它们在改善血脂异常、系统性炎症和肠道菌群失调方面也表现出相似的效果。结肠屏障完整性的基因显著上调，肝脏脂质代谢和结肠炎症反应的基因受到抑制。它们减轻了肥胖小鼠的肠道菌群失调，如有益菌（双歧杆菌和奥尔森氏菌）的显著富集和有害菌（黏液螺旋菌和幽门螺旋杆菌）的抑制。通过给予 ASKP、60P 和 60S，还观察到与短链脂肪酸产生促进和与肥胖和肠道菌群失调相关的代谢物（缬氨酸、亮氨酸和异亮氨酸生物合成和氮代谢）减少相关的碳水化合物代谢的显著富集。总之，这些多糖具有作为预防高脂肪饮食诱导肥胖的益生元的潜力。
