内科学
内分泌学
塞德
肥胖
粪便
粪便细菌疗法
移植
肠道菌群
碳水化合物代谢
饮食性肥胖
医学
生物
免疫学
胰岛素抵抗
生物化学
艰难梭菌
抗生素
古生物学
作者
Jereon Zoll,Mark Read,Sarah Heywood,Emma Estévez,Jessica P. Marshall,Hélène L. Kammoun,Tamara L. Allen,Andrew Holmes,Mark A. Febbraio,Darren C. Henstridge
出处
期刊:American Journal of Physiology-endocrinology and Metabolism
[American Physiological Society]
日期:2020-07-01
卷期号:319 (1): E203-E216
被引量:26
标识
DOI:10.1152/ajpendo.00037.2020
摘要
Studies suggest the gut microbiota contributes to the development of obesity and metabolic syndrome. Exercise alters microbiota composition and diversity and is protective of these maladies. We tested whether the protective metabolic effects of exercise are mediated through fecal components through assessment of body composition and metabolism in recipients of fecal microbiota transplantation (FMT) from exercise-trained (ET) mice fed normal or high-energy diets. Donor C57BL/6J mice were fed a chow or high-fat, high-sucrose diet (HFHS) for 4 wk to induce obesity and glucose intolerance. Mice were divided into sedentary (Sed) or ET groups (6 wk treadmill-based ET) while maintaining their diets, resulting in four donor groups: chow sedentary (NC-Sed) or ET (NC-ET) and HFHS sedentary (HFHS-Sed) or ET (HFHS-ET). Chow-fed recipient mice were gavaged with feces from the respective donor groups weekly, creating four groups (NC-Sed-R, NC-ET-R, HFHS-Sed-R, HFHS-ET-R), and body composition and metabolism were assessed. The HFHS diet led to glucose intolerance and obesity in the donors, whereas exercise training (ET) restrained adiposity and improved glucose tolerance. No donor group FMT altered recipient body composition. Despite unaltered adiposity, glucose levels were disrupted when challenged in mice receiving feces from HFHS-fed donors, irrespective of donor-ET status, with a decrease in insulin-stimulated glucose clearance into white adipose tissue and large intestine and specific changes in the recipient’s microbiota composition observed. FMT can transmit HFHS-induced disrupted glucose metabolism to recipient mice independently of any change in adiposity. However, the protective metabolic effect of ET on glucose metabolism is not mediated through fecal factors.
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