Compositional and Functional Adaptations of Intestinal Microbiota and Related Metabolites in CKD Patients Receiving Dietary Protein Restriction
The relationship between change of gut microbiota and host serum metabolomics associated with low protein diet (LPD) has been unraveled incompletely in CKD patients. Fecal 16S rRNA gene sequencing and serum metabolomics profiling were performed. We reported significant changes in the β-diversity of...
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| Vydané v: | Nutrients Ročník 12; číslo 9; s. 2799 |
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| Abstract | The relationship between change of gut microbiota and host serum metabolomics associated with low protein diet (LPD) has been unraveled incompletely in CKD patients. Fecal 16S rRNA gene sequencing and serum metabolomics profiling were performed. We reported significant changes in the β-diversity of gut microbiota in CKD patients having LPD (CKD-LPD, n = 16). We identified 19 genera and 12 species with significant differences in their relative abundance among CKD-LPD patients compared to patients receiving normal protein diet (CKD-NPD, n = 27) or non-CKD controls (n = 34), respectively. CKD-LPD had a significant decrease in the abundance of many butyrate-producing bacteria (family Lachnospiraceae and Bacteroidaceae) associated with enrichment of functional module of butanoate metabolism, leading to concomitant reduction in serum levels of SCFA (acetic, heptanoic and nonanoic acid). A secondary bile acid, glyco λ-muricholic acid, was significantly increased in CKD-LPD patients. Serum levels of indoxyl sulfate and p-cresyl sulfate did not differ among groups. The relationship between abundances of microbes and metabolites remained significant in subset of resampling subjects of comparable characteristics. Enrichment of bacterial gene markers related to D-alanine, ketone bodies and glutathione metabolism was noted in CKD-LPD patients. Our analyses reveal signatures and functions of gut microbiota to adapt dietary protein restriction in renal patients. |
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| AbstractList | The relationship between change of gut microbiota and host serum metabolomics associated with low protein diet (LPD) has been unraveled incompletely in CKD patients. Fecal 16S rRNA gene sequencing and serum metabolomics profiling were performed. We reported significant changes in the β-diversity of gut microbiota in CKD patients having LPD (CKD-LPD, n = 16). We identified 19 genera and 12 species with significant differences in their relative abundance among CKD-LPD patients compared to patients receiving normal protein diet (CKD-NPD, n = 27) or non-CKD controls (n = 34), respectively. CKD-LPD had a significant decrease in the abundance of many butyrate-producing bacteria (family Lachnospiraceae and Bacteroidaceae) associated with enrichment of functional module of butanoate metabolism, leading to concomitant reduction in serum levels of SCFA (acetic, heptanoic and nonanoic acid). A secondary bile acid, glyco λ-muricholic acid, was significantly increased in CKD-LPD patients. Serum levels of indoxyl sulfate and p-cresyl sulfate did not differ among groups. The relationship between abundances of microbes and metabolites remained significant in subset of resampling subjects of comparable characteristics. Enrichment of bacterial gene markers related to D-alanine, ketone bodies and glutathione metabolism was noted in CKD-LPD patients. Our analyses reveal signatures and functions of gut microbiota to adapt dietary protein restriction in renal patients. The relationship between change of gut microbiota and host serum metabolomics associated with low protein diet (LPD) has been unraveled incompletely in CKD patients. Fecal 16S rRNA gene sequencing and serum metabolomics profiling were performed. We reported significant changes in the β-diversity of gut microbiota in CKD patients having LPD (CKD-LPD, = 16). We identified 19 genera and 12 species with significant differences in their relative abundance among CKD-LPD patients compared to patients receiving normal protein diet (CKD-NPD, = 27) or non-CKD controls ( = 34), respectively. CKD-LPD had a significant decrease in the abundance of many butyrate-producing bacteria (family and ) associated with enrichment of functional module of butanoate metabolism, leading to concomitant reduction in serum levels of SCFA (acetic, heptanoic and nonanoic acid). A secondary bile acid, glyco λ-muricholic acid, was significantly increased in CKD-LPD patients. Serum levels of indoxyl sulfate and p-cresyl sulfate did not differ among groups. The relationship between abundances of microbes and metabolites remained significant in subset of resampling subjects of comparable characteristics. Enrichment of bacterial gene markers related to D-alanine, ketone bodies and glutathione metabolism was noted in CKD-LPD patients. Our analyses reveal signatures and functions of gut microbiota to adapt dietary protein restriction in renal patients. The relationship between change of gut microbiota and host serum metabolomics associated with low protein diet (LPD) has been unraveled incompletely in CKD patients. Fecal 16S rRNA gene sequencing and serum metabolomics profiling were performed. We reported significant changes in the β-diversity of gut microbiota in CKD patients having LPD (CKD-LPD, n = 16). We identified 19 genera and 12 species with significant differences in their relative abundance among CKD-LPD patients compared to patients receiving normal protein diet (CKD-NPD, n = 27) or non-CKD controls (n = 34), respectively. CKD-LPD had a significant decrease in the abundance of many butyrate-producing bacteria (family Lachnospiraceae and Bacteroidaceae) associated with enrichment of functional module of butanoate metabolism, leading to concomitant reduction in serum levels of SCFA (acetic, heptanoic and nonanoic acid). A secondary bile acid, glyco λ-muricholic acid, was significantly increased in CKD-LPD patients. Serum levels of indoxyl sulfate and p-cresyl sulfate did not differ among groups. The relationship between abundances of microbes and metabolites remained significant in subset of resampling subjects of comparable characteristics. Enrichment of bacterial gene markers related to D-alanine, ketone bodies and glutathione metabolism was noted in CKD-LPD patients. Our analyses reveal signatures and functions of gut microbiota to adapt dietary protein restriction in renal patients.The relationship between change of gut microbiota and host serum metabolomics associated with low protein diet (LPD) has been unraveled incompletely in CKD patients. Fecal 16S rRNA gene sequencing and serum metabolomics profiling were performed. We reported significant changes in the β-diversity of gut microbiota in CKD patients having LPD (CKD-LPD, n = 16). We identified 19 genera and 12 species with significant differences in their relative abundance among CKD-LPD patients compared to patients receiving normal protein diet (CKD-NPD, n = 27) or non-CKD controls (n = 34), respectively. CKD-LPD had a significant decrease in the abundance of many butyrate-producing bacteria (family Lachnospiraceae and Bacteroidaceae) associated with enrichment of functional module of butanoate metabolism, leading to concomitant reduction in serum levels of SCFA (acetic, heptanoic and nonanoic acid). A secondary bile acid, glyco λ-muricholic acid, was significantly increased in CKD-LPD patients. Serum levels of indoxyl sulfate and p-cresyl sulfate did not differ among groups. The relationship between abundances of microbes and metabolites remained significant in subset of resampling subjects of comparable characteristics. Enrichment of bacterial gene markers related to D-alanine, ketone bodies and glutathione metabolism was noted in CKD-LPD patients. Our analyses reveal signatures and functions of gut microbiota to adapt dietary protein restriction in renal patients. |
| Author | Yang, Chi-Wei Su, Shih-Chi Hsu, Heng-Jung Lai, Hsin-Chih Chang, Lun-Ching Sun, Chiao-Yin Wu, I-Wen Lee, Chin-Chan Chen, Yuen-Chan Yang, Kai-Jie Chung, Wen-Hun |
| AuthorAffiliation | 5 Department of Medical Biotechnology and Laboratory Science and Microbiota Research Center, College of Medicine, Chang Gung University, Taoyuan 333, Taiwan; hclai@mail.cgu.edu.tw 4 Whole-Genome Research Core Laboratory of Human Diseases, Chang Gung Memorial Hospital, Keelung 20401, Taiwan; chung1@cgmh.org.tw 7 Department of Dermatology, Drug Hypersensitivity Clinical and Research Center, Chang Gung Memorial Hospital, Linkou 33305, Taiwan 6 Department of Mathematical Sciences, Florida Atlantic University, Boca Raton, FL 33431, USA 1 Department of Nephrology, Chang Gung Memorial Hospital, Keelung 20401, Taiwan; fliawu@yahoo.com (I.-W.W.); leefang@cgmh.org.tw (C.-C.L.); r5267@cgmh.org.tw (H.-J.H.); fish3970@gmail.com (C.-Y.S.); eva90156@cgmh.org.tw (K.-J.Y.) 3 Kidney Research Center, Department of Nephrology, Chang Gung Memorial Hospital, Linkuo 33305, Taiwan 2 College of Medicine, Chang Gung University, Taoyuan 33305, Taiwan; cyc2356@cgmh.org.tw (Y.-C.C.); cwyang00@gmail.com (C.-W.Y.) |
| AuthorAffiliation_xml | – name: 1 Department of Nephrology, Chang Gung Memorial Hospital, Keelung 20401, Taiwan; fliawu@yahoo.com (I.-W.W.); leefang@cgmh.org.tw (C.-C.L.); r5267@cgmh.org.tw (H.-J.H.); fish3970@gmail.com (C.-Y.S.); eva90156@cgmh.org.tw (K.-J.Y.) – name: 2 College of Medicine, Chang Gung University, Taoyuan 33305, Taiwan; cyc2356@cgmh.org.tw (Y.-C.C.); cwyang00@gmail.com (C.-W.Y.) – name: 3 Kidney Research Center, Department of Nephrology, Chang Gung Memorial Hospital, Linkuo 33305, Taiwan – name: 6 Department of Mathematical Sciences, Florida Atlantic University, Boca Raton, FL 33431, USA – name: 4 Whole-Genome Research Core Laboratory of Human Diseases, Chang Gung Memorial Hospital, Keelung 20401, Taiwan; chung1@cgmh.org.tw – name: 5 Department of Medical Biotechnology and Laboratory Science and Microbiota Research Center, College of Medicine, Chang Gung University, Taoyuan 333, Taiwan; hclai@mail.cgu.edu.tw – name: 7 Department of Dermatology, Drug Hypersensitivity Clinical and Research Center, Chang Gung Memorial Hospital, Linkou 33305, Taiwan |
| Author_xml | – sequence: 1 givenname: I-Wen orcidid: 0000-0001-8535-3582 surname: Wu fullname: Wu, I-Wen – sequence: 2 givenname: Chin-Chan orcidid: 0000-0003-1165-095X surname: Lee fullname: Lee, Chin-Chan – sequence: 3 givenname: Heng-Jung surname: Hsu fullname: Hsu, Heng-Jung – sequence: 4 givenname: Chiao-Yin surname: Sun fullname: Sun, Chiao-Yin – sequence: 5 givenname: Yuen-Chan surname: Chen fullname: Chen, Yuen-Chan – sequence: 6 givenname: Kai-Jie surname: Yang fullname: Yang, Kai-Jie – sequence: 7 givenname: Chi-Wei surname: Yang fullname: Yang, Chi-Wei – sequence: 8 givenname: Wen-Hun surname: Chung fullname: Chung, Wen-Hun – sequence: 9 givenname: Hsin-Chih surname: Lai fullname: Lai, Hsin-Chih – sequence: 10 givenname: Lun-Ching orcidid: 0000-0002-8039-5350 surname: Chang fullname: Chang, Lun-Ching – sequence: 11 givenname: Shih-Chi surname: Su fullname: Su, Shih-Chi |
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| Keywords | low protein diet uremic solute chronic kidney disease gut microbiome short-chain fatty acids bile acids |
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| SubjectTerms | Adaptation, Physiological Aged Bacteroidaceae bile acids Bile Acids and Salts - metabolism blood serum butyrates Diet Diet, Protein-Restricted - methods dietary protein Dietitians Discriminant analysis Fatty acids Feces - microbiology Female Gastrointestinal Microbiome - physiology genes Glomerular Filtration Rate glutathione Humans intestinal microorganisms Lachnospiraceae low protein diet Male metabolism Metabolites Metabolome - physiology Metabolomics Microbiota Middle Aged pelargonic acid Phylogenetics Probiotics Proteins Renal Insufficiency, Chronic - diet therapy Renal Insufficiency, Chronic - metabolism Renal Insufficiency, Chronic - microbiology RNA, Ribosomal, 16S Software sulfates Vegetarianism |
| Title | Compositional and Functional Adaptations of Intestinal Microbiota and Related Metabolites in CKD Patients Receiving Dietary Protein Restriction |
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