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衍生丙基丙烷硫代亚磺酸盐在饮食诱导肥胖的小鼠模型中发挥抗肥胖作用。

The Derivate Propyl Propane Thiosulfinate Exerts Anti-Obesogenic Effects in a Murine Model of Diet-Induced Obesity.

作者信息

Liébana-García Rebeca, Olivares Marta, Rodríguez-Ruano Sonia M, Tolosa-Enguís Verónica, Chulia Isabel, Gil-Martínez Lidia, Guillamón Enrique, Baños Alberto, Sanz Yolanda

机构信息

Institute of Agrochemistry and Food Technology, Spanish National Research Council (IATA-CSIC), 46980 Valencia, Spain.

Department of Microbiology, Faculty of Sciences, University of Granada, 18011 Granada, Spain.

出版信息

Nutrients. 2022 Jan 19;14(3):440. doi: 10.3390/nu14030440.

Abstract

species and their organosulfur-derived compounds could prevent obesity and metabolic dysfunction, as they exhibit immunomodulatory and antimicrobial properties. Here, we report the anti-obesogenic potential and dose-dependent effects (0.1 or 1 mg/kg/day) of propyl propane thiosulfinate (PTS) in a murine model of diet-induced obesity. The obesogenic diet increased body weight gain and adipocyte size, and boosted inflammatory marker () expression in the adipose tissue. Conversely, PTS prevented these effects in a dose-dependent manner. Moreover, the higher dose of PTS improved glucose and hepatic homeostasis, modulated lipid metabolism, and raised markers of the thermogenic capacity of brown adipose tissue. In the colon, the obesogenic diet reduced IL-22 levels and increased gut barrier function markers (); however, the highest PTS dose normalized all of these markers to the levels of mice fed a standard diet. Gut microbiota analyses revealed no differences in diversity indexes and only minor taxonomic changes, such as an increase in butyrate producers, and , and a decrease in in mice receiving the highest PTS dose. In summary, our study provides preclinical evidence for the protective effects of PTS against obesity, which if confirmed in humans, might provide a novel plant-based dietary product to counteract this condition.

摘要

某些物种及其衍生的有机硫化合物可预防肥胖和代谢功能障碍,因为它们具有免疫调节和抗菌特性。在此,我们报告了丙基丙烷硫代亚磺酸盐(PTS)在饮食诱导肥胖小鼠模型中的抗肥胖潜力和剂量依赖性效应(0.1或1毫克/千克/天)。致肥胖饮食增加了体重增加和脂肪细胞大小,并提高了脂肪组织中炎症标志物()的表达。相反,PTS以剂量依赖性方式预防了这些效应。此外,较高剂量的PTS改善了葡萄糖和肝脏稳态,调节了脂质代谢,并提高了棕色脂肪组织产热能力的标志物。在结肠中,致肥胖饮食降低了IL-22水平并增加了肠道屏障功能标志物();然而,最高剂量的PTS将所有这些标志物恢复到喂食标准饮食小鼠的水平。肠道微生物群分析显示多样性指数没有差异,只有微小的分类学变化,例如接受最高剂量PTS的小鼠中丁酸盐产生菌和的增加,以及的减少。总之,我们的研究为PTS对肥胖的保护作用提供了临床前证据,如果在人类中得到证实,可能会提供一种新型的植物性饮食产品来对抗这种情况。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53c6/8839906/3df13e8b4e17/nutrients-14-00440-g001.jpg

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