Jian Gao1, Xiaoyu Guo1, Wei Wei1, Ran Li1,2, Ke Hu1, Xin Liu1, Wenbo Jiang1, Siyao Liu3,4, Weiqi Wang1, Hu Sun1, Huanyu Wu1, Yuntao Zhang1, Wenbo Gu1, Ying Li1,5,6, Changhao Sun7, Tianshu Han7,8. 1. Department of Nutrition and Food Hygiene, National Key Discipline, School of Public Health, Harbin Medical University, Harbin, China. 2. Harbin Center for Disease Control and Prevention, Harbin, China. 3. Division of Epidemiology, Biostatistics and Environmental Health, School of Public Health, University of Memphis, Memphis, TN. 4. Department of Epidemiology and Cancer Control, St. Jude Children's Research Hospital, Memphis, TN. 5. Key Laboratory of Hepatosplenic Surgery, Harbin Medical University, Ministry of Education, Harbin, China. 6. NHC Key Laboratory of Cell Translation, Harbin Medical University, Harbin, China. 7. Department of Nutrition and Food Hygiene, National Key Discipline, School of Public Health, Harbin Medical University, Harbin, China changhaosun2002@163.com snowcalendar@126.com. 8. Department of Endocrinology, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Abstract
OBJECTIVE: This randomized controlled-feeding trial aimed to determine the impact of fried meat intake on the gut microbiota and fecal cometabolites and whether such impacts influenced host glucose homoeostasis, intestinal endotoxin levels, and systemic inflammation. RESEARCH DESIGN AND METHODS: A total of 117 overweight adults were randomized into two groups. Fifty-nine participants were provided fried meat four times per week, and 58 participants were restricted from fried meat intake, while holding food group and nutrient compositions constant, for 4 weeks. The gut microbiota was analyzed by 16S rRNA sequencing. Glucose and insulin concentrations at 0, 30, 60, and 120 min of an oral glucose tolerance test, fecal microbiota-host cometabolite levels, and intestinal endotoxin and inflammation serum biomarker levels were measured. The area under the curve (AUC) for insulin, insulinogenic index (IGI), and muscle insulin resistance index (MIRI) were calculated. RESULTS: The participants who consumed fried meat had lower IGI values than the control subjects, but they had higher MIRI and AUC values of insulin and lipopolysaccharide (LPS), TNF-α, IL-10, and IL-1β levels (P < 0.05). Fried meat intake lowered microbial community richness and decreased Lachnospiraceae and Flavonifractor abundances while increasing Dialister, Dorea, and Veillonella abundances (P FDR <0.05), provoking a significant shift in the fecal cometabolite profile, with lower 3-indolepropionic acid, valeric acid, and butyric acid concentrations and higher carnitine and methylglutaric acid concentrations (P FDR <0.05). Changes in these cometabolite levels were significantly associated with changes in IGI and MIRI values and LPS, FGF21, TNF-α, IL-1β, and IL-10 levels (P < 0.05). CONCLUSIONS:Fried meat intake impaired glucose homoeostasis and increased intestinal endotoxin and systemic inflammation levels by influencing the gut microbiota and microbial-host cometabolites.
RCT Entities:
OBJECTIVE: This randomized controlled-feeding trial aimed to determine the impact of fried meat intake on the gut microbiota and fecal cometabolites and whether such impacts influenced host glucose homoeostasis, intestinal endotoxin levels, and systemic inflammation. RESEARCH DESIGN AND METHODS: A total of 117 overweight adults were randomized into two groups. Fifty-nine participants were provided fried meat four times per week, and 58 participants were restricted from fried meat intake, while holding food group and nutrient compositions constant, for 4 weeks. The gut microbiota was analyzed by 16S rRNA sequencing. Glucose and insulin concentrations at 0, 30, 60, and 120 min of an oral glucose tolerance test, fecal microbiota-host cometabolite levels, and intestinal endotoxin and inflammation serum biomarker levels were measured. The area under the curve (AUC) for insulin, insulinogenic index (IGI), and muscle insulin resistance index (MIRI) were calculated. RESULTS: The participants who consumed fried meat had lower IGI values than the control subjects, but they had higher MIRI and AUC values of insulin and lipopolysaccharide (LPS), TNF-α, IL-10, and IL-1β levels (P < 0.05). Fried meat intake lowered microbial community richness and decreased Lachnospiraceae and Flavonifractor abundances while increasing Dialister, Dorea, and Veillonella abundances (P FDR <0.05), provoking a significant shift in the fecal cometabolite profile, with lower 3-indolepropionic acid, valeric acid, and butyric acid concentrations and higher carnitine and methylglutaric acid concentrations (P FDR <0.05). Changes in these cometabolite levels were significantly associated with changes in IGI and MIRI values and LPS, FGF21, TNF-α, IL-1β, and IL-10 levels (P < 0.05). CONCLUSIONS: Fried meat intake impaired glucose homoeostasis and increased intestinal endotoxin and systemic inflammation levels by influencing the gut microbiota and microbial-host cometabolites.
Authors: Lina Tingö; Ashley N Hutchinson; Cecilia Bergh; Lena Stiefvatter; Anna Schweinlin; Morten G Jensen; Kirsten Krüger; Stephan C Bischoff; Robert J Brummer Journal: Nutrients Date: 2022-09-27 Impact factor: 6.706