Cheng Kong1, Renyuan Gao1, Xuebing Yan1, Linsheng Huang1, Huanlong Qin2. 1. Department of General Surgery, Shanghai 10th People's Hospital, Tongji University, Shanghai, China; Research Institute of Intestinal Diseases, Tongji University School of Medicine, Shanghai, China. 2. Department of General Surgery, Shanghai 10th People's Hospital, Tongji University, Shanghai, China; Research Institute of Intestinal Diseases, Tongji University School of Medicine, Shanghai, China. Electronic address: huanlongqin@yeah.net.
Abstract
OBJECTIVE: Gut microbiota plays a crucial role in host energy homeostasis, which is affected by both high-fat diets (HFDs) and high-sucrose diets (HCDs). Probiotics treatment can effectively modulate intestinal microbiota. However, it remains unclear whether probiotics can effectively improve HFD- and HCD-induced microbiota dysbiosis. METHODS: Mice were fed either an HFD, HCD, or normal diet for 13 wk and administered probiotics during the last 4 wk of the diet. Fecal and cecal samples were collected and analyzed by high-throughput 16S ribosomal RNA sequencing. RESULTS: Body weight increased more in the HFD group compared with the HCD group. Probiotics supplementation slowed weight gain in both the HFD and HCD groups. Both the HFD and HCD reduced microbial diversity, abundance of butyric acid-producing bacteria, and some other beneficial bacteria, including Lactobacillus, Clostridium sensu stricto, Prevotella, and Alloprevotella, but increased conditional pathogenic bacteria, such as Bacteroides, Alistipes, and Anaerotruncus. Probiotics markedly restored the proportions of bacteria affected in the HFD and HCD groups and increased the abundance of microbiota negatively associated with obesity, including Bifidobacterium, Lactococcus, and Akkermansia. In addition, Oscillibacter, Escherichia/Shigella, Acinetobacter, and Blautia significantly increased in the HCD group; Allobaculum, Olsenella, and Ruminococcus were significantly changed in the HFD group. HCD-induced microbiota dysbiosis was more susceptible to probiotics treatment compared with the HFD. CONCLUSIONS: Probiotics treatment can mitigate diet-induced obesity partly through modulating intestinal microbiota, especially in HCD-induced obesity.
OBJECTIVE: Gut microbiota plays a crucial role in host energy homeostasis, which is affected by both high-fat diets (HFDs) and high-sucrose diets (HCDs). Probiotics treatment can effectively modulate intestinal microbiota. However, it remains unclear whether probiotics can effectively improve HFD- and HCD-induced microbiota dysbiosis. METHODS:Mice were fed either an HFD, HCD, or normal diet for 13 wk and administered probiotics during the last 4 wk of the diet. Fecal and cecal samples were collected and analyzed by high-throughput 16S ribosomal RNA sequencing. RESULTS: Body weight increased more in the HFD group compared with the HCD group. Probiotics supplementation slowed weight gain in both the HFD and HCD groups. Both the HFD and HCD reduced microbial diversity, abundance of butyric acid-producing bacteria, and some other beneficial bacteria, including Lactobacillus, Clostridium sensu stricto, Prevotella, and Alloprevotella, but increased conditional pathogenic bacteria, such as Bacteroides, Alistipes, and Anaerotruncus. Probiotics markedly restored the proportions of bacteria affected in the HFD and HCD groups and increased the abundance of microbiota negatively associated with obesity, including Bifidobacterium, Lactococcus, and Akkermansia. In addition, Oscillibacter, Escherichia/Shigella, Acinetobacter, and Blautia significantly increased in the HCD group; Allobaculum, Olsenella, and Ruminococcus were significantly changed in the HFD group. HCD-induced microbiota dysbiosis was more susceptible to probiotics treatment compared with the HFD. CONCLUSIONS: Probiotics treatment can mitigate diet-induced obesity partly through modulating intestinal microbiota, especially in HCD-induced obesity.
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