Parabacteroides distasonis Alleviates Obesity and Metabolic Dysfunctions via Production of Succinate and Secondary Bile Acids
We demonstrated the metabolic benefits of Parabacteroides distasonis (PD) on decreasing weight gain, hyperglycemia, and hepatic steatosis in ob/ob and high-fat diet (HFD)-fed mice. Treatment with live P. distasonis (LPD) dramatically altered the bile acid profile with elevated lithocholic acid (LCA)...
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| Published in | Cell reports (Cambridge) Vol. 26; no. 1; pp. 222 - 235.e5 |
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| Main Authors | , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Elsevier Inc
02.01.2019
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| Subjects | |
| Online Access | Get full text |
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| Abstract | We demonstrated the metabolic benefits of Parabacteroides distasonis (PD) on decreasing weight gain, hyperglycemia, and hepatic steatosis in ob/ob and high-fat diet (HFD)-fed mice. Treatment with live P. distasonis (LPD) dramatically altered the bile acid profile with elevated lithocholic acid (LCA) and ursodeoxycholic acid (UDCA) and increased the level of succinate in the gut. In vitro cultivation of PD demonstrated its capacity to transform bile acids and production of succinate. Succinate supplementation in the diet decreased hyperglycemia in ob/ob mice via the activation of intestinal gluconeogenesis (IGN). Gavage with a mixture of LCA and UDCA reduced hyperlipidemia by activating the FXR pathway and repairing gut barrier integrity. Co-treatment with succinate and LCA/UDCA mirrored the benefits of LPD. The binding target of succinate was identified as fructose-1,6-bisphosphatase, the rate-limiting enzyme in IGN. The succinate and secondary bile acids produced by P. distasonis played key roles in the modulation of host metabolism.
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•Parabacteroides distasonis alleviates obesity and obesity-related dysfunctions in mice.•P. distasonis generates succinate and secondary bile acids in the gut.•P. distasonis activates intestinal gluconeogenesis (IGN) and FXR pathways in the gut.•Succinate is a ligand of fructose-1,6-bisphosphatase, the rate-limiting enzyme in IGN.
Wang et al. report the metabolic benefits of gut commensal Parabacteroides distasonis via secondary bile acid-activated FXR signaling and succinate-activated intestinal gluconeogenesis (IGN). Succinate binds fructose-1,6-bisphosphatase, the rate-limiting enzyme in IGN. |
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| AbstractList | We demonstrated the metabolic benefits of Parabacteroides distasonis (PD) on decreasing weight gain, hyperglycemia, and hepatic steatosis in ob/ob and high-fat diet (HFD)-fed mice. Treatment with live P. distasonis (LPD) dramatically altered the bile acid profile with elevated lithocholic acid (LCA) and ursodeoxycholic acid (UDCA) and increased the level of succinate in the gut. In vitro cultivation of PD demonstrated its capacity to transform bile acids and production of succinate. Succinate supplementation in the diet decreased hyperglycemia in ob/ob mice via the activation of intestinal gluconeogenesis (IGN). Gavage with a mixture of LCA and UDCA reduced hyperlipidemia by activating the FXR pathway and repairing gut barrier integrity. Co-treatment with succinate and LCA/UDCA mirrored the benefits of LPD. The binding target of succinate was identified as fructose-1,6-bisphosphatase, the rate-limiting enzyme in IGN. The succinate and secondary bile acids produced by P. distasonis played key roles in the modulation of host metabolism. We demonstrated the metabolic benefits of Parabacteroides distasonis (PD) on decreasing weight gain, hyperglycemia, and hepatic steatosis in ob/ob and high-fat diet (HFD)-fed mice. Treatment with live P. distasonis (LPD) dramatically altered the bile acid profile with elevated lithocholic acid (LCA) and ursodeoxycholic acid (UDCA) and increased the level of succinate in the gut. In vitro cultivation of PD demonstrated its capacity to transform bile acids and production of succinate. Succinate supplementation in the diet decreased hyperglycemia in ob/ob mice via the activation of intestinal gluconeogenesis (IGN). Gavage with a mixture of LCA and UDCA reduced hyperlipidemia by activating the FXR pathway and repairing gut barrier integrity. Co-treatment with succinate and LCA/UDCA mirrored the benefits of LPD. The binding target of succinate was identified as fructose-1,6-bisphosphatase, the rate-limiting enzyme in IGN. The succinate and secondary bile acids produced by P. distasonis played key roles in the modulation of host metabolism.We demonstrated the metabolic benefits of Parabacteroides distasonis (PD) on decreasing weight gain, hyperglycemia, and hepatic steatosis in ob/ob and high-fat diet (HFD)-fed mice. Treatment with live P. distasonis (LPD) dramatically altered the bile acid profile with elevated lithocholic acid (LCA) and ursodeoxycholic acid (UDCA) and increased the level of succinate in the gut. In vitro cultivation of PD demonstrated its capacity to transform bile acids and production of succinate. Succinate supplementation in the diet decreased hyperglycemia in ob/ob mice via the activation of intestinal gluconeogenesis (IGN). Gavage with a mixture of LCA and UDCA reduced hyperlipidemia by activating the FXR pathway and repairing gut barrier integrity. Co-treatment with succinate and LCA/UDCA mirrored the benefits of LPD. The binding target of succinate was identified as fructose-1,6-bisphosphatase, the rate-limiting enzyme in IGN. The succinate and secondary bile acids produced by P. distasonis played key roles in the modulation of host metabolism. We demonstrated the metabolic benefits of Parabacteroides distasonis (PD) on decreasing weight gain, hyperglycemia, and hepatic steatosis in ob/ob and high-fat diet (HFD)-fed mice. Treatment with live P. distasonis (LPD) dramatically altered the bile acid profile with elevated lithocholic acid (LCA) and ursodeoxycholic acid (UDCA) and increased the level of succinate in the gut. In vitro cultivation of PD demonstrated its capacity to transform bile acids and production of succinate. Succinate supplementation in the diet decreased hyperglycemia in ob/ob mice via the activation of intestinal gluconeogenesis (IGN). Gavage with a mixture of LCA and UDCA reduced hyperlipidemia by activating the FXR pathway and repairing gut barrier integrity. Co-treatment with succinate and LCA/UDCA mirrored the benefits of LPD. The binding target of succinate was identified as fructose-1,6-bisphosphatase, the rate-limiting enzyme in IGN. The succinate and secondary bile acids produced by P. distasonis played key roles in the modulation of host metabolism. [Display omitted] •Parabacteroides distasonis alleviates obesity and obesity-related dysfunctions in mice.•P. distasonis generates succinate and secondary bile acids in the gut.•P. distasonis activates intestinal gluconeogenesis (IGN) and FXR pathways in the gut.•Succinate is a ligand of fructose-1,6-bisphosphatase, the rate-limiting enzyme in IGN. Wang et al. report the metabolic benefits of gut commensal Parabacteroides distasonis via secondary bile acid-activated FXR signaling and succinate-activated intestinal gluconeogenesis (IGN). Succinate binds fructose-1,6-bisphosphatase, the rate-limiting enzyme in IGN. |
| Author | Zheng, Zhongyong Wang, Yujing Ma, Ke Liu, Hongwei Bao, Li Wang, Wenzhao Wang, Kai Zhou, Nan Wang, Jun Liao, Mingfang Liu, Shuang-Jiang Liu, Chang |
| Author_xml | – sequence: 1 givenname: Kai surname: Wang fullname: Wang, Kai organization: State Key Laboratory of Mycology, Institute of Microbiology, Chinese Academy of Sciences, No. 1 Beichenxi Road, Chaoyang District, Beijing 100101, People’s Republic of China – sequence: 2 givenname: Mingfang surname: Liao fullname: Liao, Mingfang organization: State Key Laboratory of Mycology, Institute of Microbiology, Chinese Academy of Sciences, No. 1 Beichenxi Road, Chaoyang District, Beijing 100101, People’s Republic of China – sequence: 3 givenname: Nan surname: Zhou fullname: Zhou, Nan organization: State Key Laboratory of Microbial Resources, Institute of Microbiology, Chinese Academy of Sciences, No. 1 Beichenxi Road, Chaoyang District, Beijing 100101, People’s Republic of China – sequence: 4 givenname: Li surname: Bao fullname: Bao, Li organization: State Key Laboratory of Mycology, Institute of Microbiology, Chinese Academy of Sciences, No. 1 Beichenxi Road, Chaoyang District, Beijing 100101, People’s Republic of China – sequence: 5 givenname: Ke surname: Ma fullname: Ma, Ke organization: State Key Laboratory of Mycology, Institute of Microbiology, Chinese Academy of Sciences, No. 1 Beichenxi Road, Chaoyang District, Beijing 100101, People’s Republic of China – sequence: 6 givenname: Zhongyong surname: Zheng fullname: Zheng, Zhongyong organization: State Key Laboratory of Mycology, Institute of Microbiology, Chinese Academy of Sciences, No. 1 Beichenxi Road, Chaoyang District, Beijing 100101, People’s Republic of China – sequence: 7 givenname: Yujing surname: Wang fullname: Wang, Yujing organization: Savaid Medical School, University of Chinese Academy of Sciences, Beijing 100049, People’s Republic of China – sequence: 8 givenname: Chang surname: Liu fullname: Liu, Chang organization: State Key Laboratory of Microbial Resources, Institute of Microbiology, Chinese Academy of Sciences, No. 1 Beichenxi Road, Chaoyang District, Beijing 100101, People’s Republic of China – sequence: 9 givenname: Wenzhao surname: Wang fullname: Wang, Wenzhao organization: State Key Laboratory of Mycology, Institute of Microbiology, Chinese Academy of Sciences, No. 1 Beichenxi Road, Chaoyang District, Beijing 100101, People’s Republic of China – sequence: 10 givenname: Jun surname: Wang fullname: Wang, Jun organization: CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, No. 1 Beichenxi Road, Chaoyang District, Beijing 100101, People’s Republic of China – sequence: 11 givenname: Shuang-Jiang surname: Liu fullname: Liu, Shuang-Jiang email: liusj@im.ac.cn organization: Savaid Medical School, University of Chinese Academy of Sciences, Beijing 100049, People’s Republic of China – sequence: 12 givenname: Hongwei surname: Liu fullname: Liu, Hongwei email: liuhw@im.ac.cn organization: State Key Laboratory of Mycology, Institute of Microbiology, Chinese Academy of Sciences, No. 1 Beichenxi Road, Chaoyang District, Beijing 100101, People’s Republic of China |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/30605678$$D View this record in MEDLINE/PubMed |
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| Keywords | succinate Parabacteroides distasonis metabolic disorders FBPase bile acids |
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| SubjectTerms | Animals Bacterial Proteins - chemistry Bacteroidetes - enzymology bile acids Bile Acids and Salts - metabolism FBPase Gastrointestinal Microbiome - physiology Humans metabolic disorders Mice Obesity - microbiology Parabacteroides distasonis succinate Succinic Acid - metabolism |
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| Title | Parabacteroides distasonis Alleviates Obesity and Metabolic Dysfunctions via Production of Succinate and Secondary Bile Acids |
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