| Autor: |
Trikha SRJ; Department of Food Science & Human Nutrition, Colorado State University, Fort Collins, CO, USA., Lee DM; Department of Nutritional Medicine, Brooke Army Medical Center, San Antonio, TX, USA., Ecton KE; Department of Food Science & Human Nutrition, Colorado State University, Fort Collins, CO, USA., Wrigley SD; Department of Food Science & Human Nutrition, Colorado State University, Fort Collins, CO, USA., Vazquez AR; Department of Food Science & Human Nutrition, Colorado State University, Fort Collins, CO, USA., Litwin NS; Center for Microbiome Innovation, University of California San Diego, La Jolla, CA, USA., Thomas KN; Department of Food Science & Human Nutrition, Colorado State University, Fort Collins, CO, USA., Wei Y; Department of Food Science & Human Nutrition, Colorado State University, Fort Collins, CO, USA., Battson ML; Department of Nutrition, Metropolitan State University, Denver, CO, USA., Johnson SA; Department of Food Science & Human Nutrition, Colorado State University, Fort Collins, CO, USA., Kuhn KA; School of Medicine in the Division of Rheumatology and Gnotobiotic Core Director, University of Colorado School of Medicine, Aurora, CO, USA., Colgan SP; School of Medicine in the Division of Gastroenterology and Hepatology, University of Colorado School of Medicine, Aurora, CO, USA., Gentile CL; Department of Food Science & Human Nutrition, Colorado State University, Fort Collins, CO, USA., Weir TL; Department of Food Science & Human Nutrition, Colorado State University, Fort Collins, CO, USA. |
| Abstrakt: |
Recent preclinical data suggest that alterations in the gut microbiota may be an important factor linking obesity to vascular dysfunction, an early sign of cardiovascular disease. The purpose of this study was to begin translation of these preclinical data by examining whether vascular phenotypes in humans are transmissible through the gut microbiota. We hypothesized that germ-free mice colonized with gut microbiota from obese individuals would display diminished vascular function compared to germ-free mice receiving microbiota from lean individuals.We transplanted fecal material from obese and lean age-and sex-matched participants with disparate vascular function to germ-free mice. Using Principle Component Analysis, the microbiota of colonized mice separated by donor group along the first principle component, accounting for between 70-93% of the total variability in the dataset. The microbiota of mice receiving transplants from lean individuals was also characterized by increased alpha diversity, as well as increased relative abundance of potentially beneficial bacteria, including Bifidobacterium, Lactobacillus , and Bacteroides ovatis . Endothelium-dependent dilation, aortic pulse wave velocity and glucose tolerance were significantly altered in mice receiving microbiota from the obese donor relative to those receiving microbiota from the lean donor or those remaining germ-free.These data indicate that the obesity-associated human gut microbiota is sufficient to alter the vascular phenotype in germ-free mice in the absence of differences in body weight or dietary manipulation, and provide justification for future clinical trials to test the efficacy of microbiota-targeted therapies in the prevention or treatment of cardiovascular disease. |
