School of Nutritional Sciences and Wellness, University of Arizona, ACBS Building, 1117 E Lowell Street, Tucson, AZ, 85711, USA.
KEYS Program, BIO5 Institute, University of Arizona, Tucson, USA.
Metabolomics. 2022 Jul 23;18(8):60. doi: 10.1007/s11306-022-01920-9.
Obesity occurs partly due to consumption of a high-fat, high-sugar and low fiber diet and is associated with an altered gut microbiome. Prebiotic supplementation can reverse obesity and beneficially alter the gut microbiome, evidenced by previous studies in rodents. However, the role of the small intestinal metabolome in obese and prebiotic supplemented rodents has never been investigated.
To investigate and compare the small intestinal metabolome of healthy and obese rats, as well as obese rats supplemented with the prebiotic oligofructose (OFS).
Untargeted metabolomics was performed on small intestinal contents of healthy chow-fed, high fat diet-induced obese, and obese rats supplemented with oligofructose using UPLC-MS/MS. Quantification of enterohepatic bile acids was performed with UPLC-MS to determine specific effects of obesity and fiber supplementation on the bile acid pool composition.
The small intestinal metabolome of obese rats was distinct from healthy rats. OFS supplementation did not significantly alter the small intestinal metabolome but did alter levels of several metabolites compared to obese rats, including bile acid metabolites, amino acid metabolites, and metabolites related to the gut microbiota. Further, obese rats had lower total bile acids and increased taurine-conjugated bile acid species in enterohepatic circulation; this effect was reversed with OFS supplementation in high fat-feeding.
Obesity is associated with a distinct small intestinal metabolome, and OFS supplementation reverses some metabolite levels that were altered in obese rats. Future research into the effects of specific metabolites identified in this study will provide deeper insight into the mechanism of fiber supplementation on improved body weight.
肥胖部分是由于高脂肪、高糖和低纤维饮食的摄入引起的，并且与肠道微生物群的改变有关。先前在啮齿动物中的研究表明，益生元的补充可以逆转肥胖并有益地改变肠道微生物群。然而，肥胖和补充益生元的啮齿动物的小肠代谢组学的作用从未被研究过。
研究和比较健康和肥胖大鼠以及补充益生元低聚果糖（OFS）的肥胖大鼠的小肠代谢组。
使用 UPLC-MS/MS 对健康饮食喂养、高脂肪饮食诱导肥胖和补充低聚果糖的肥胖大鼠的小肠内容物进行非靶向代谢组学分析。使用 UPLC-MS 定量测定肠肝胆汁酸，以确定肥胖和纤维补充对胆汁酸池组成的具体影响。
肥胖大鼠的小肠代谢组与健康大鼠明显不同。OFS 补充并没有显著改变小肠代谢组，但与肥胖大鼠相比，它确实改变了几种代谢物的水平，包括胆汁酸代谢物、氨基酸代谢物和与肠道微生物群相关的代谢物。此外，肥胖大鼠的总胆汁酸较低，肠肝循环中的牛磺酸结合胆汁酸种类增加；这种效应在高脂肪喂养时用 OFS 补充得到了逆转。
肥胖与明显的小肠代谢组有关，OFS 补充逆转了肥胖大鼠中改变的一些代谢物水平。对本研究中鉴定的特定代谢物的影响进行进一步研究，将深入了解纤维补充对改善体重的作用机制。
