Dataset Information

Periodontal pathogen induces entero-hepatic metabolic derangements in type 2 diabetic mouse model

ABSTRACT: This is the first report of the metabolic and metaproteomic integrated changes in the gut and liver by the swallowed periodontopathogen. Periodontal disease pathogen Porphyromonas gingivalis are observed in faeces as peptides level in proteomic analysis and make changes in bowel microbial composition in db/db mouse. Orally Periodontal disease pathogen throwing as experimental periodontal disease model make gluconeogenesis in db/db mouse liver and hyperglycemia. Multi-omics analysis reveal Pg decreasing in energy metabolism and glucagon store in db/db mouse liver. These findings suggest that periodontal treatment improving oral microbiota can make diabetic hyperglycemia ameliorate in liver and support these diabetes treatments credibly.

ORGANISM(S): Cellular Organisms

SUBMITTER: Shinya Murakami

PROVIDER: PXD021851 | JPOST Repository | Tue Sep 21 00:00:00 BST 2021

REPOSITORIES: jPOST

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Publications

Porphyromonas gingivalis induces entero-hepatic metabolic derangements with alteration of gut microbiota in a type 2 diabetes mouse model.

Kashiwagi Yoichiro Y Aburaya Shunsuke S Sugiyama Naoyuki N Narukawa Yuki Y Sakamoto Yuta Y Takahashi Masatomo M Uemura Hayato H Yamashita Rentaro R Tominaga Shotaro S Hayashi Satoko S Nozaki Takenori T Yamada Satoru S Izumi Yoshihiro Y Kashiwagi Atsunori A Bamba Takeshi T Ishihama Yasushi Y Murakami Shinya S

Scientific reports 20210915 1

Periodontal infection induces systemic inflammation; therefore, aggravating diabetes. Orally administered periodontal pathogens may directly alter the gut microbiota. We orally treated obese db/db diabetes mice using Porphyromonas gingivalis (Pg). We screened for Pg-specific peptides in the intestinal fecal specimens and examined whether Pg localization influenced the intestinal microbiota profile, in turn altering the levels of the gut metabolites. We evaluated whether the deterioration in fast ...[more]

PMID: 34526589

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Project description:Dyslipidemia is a significant risk factor for progression of diabetic kidney disease (DKD). To identify individual lipids and lipid networks that may be involved in DKD progression, we performed untargeted lipidomic analysis of kidney cortex tissue from diabetic db/db and db/db eNOS-/- mice along with nondiabetic littermate controls. A subset of mice were treated with the renin-angiotensin system (RAS) inhibitors, lisinopril and losartan, which improves the DKD phenotype in the db/db eNOS-/- mouse model. Of the three independent variables in this study, diabetes had the largest impact on overall lipid levels in the kidney cortex, while eNOS expression and RAS inhibition had smaller impacts on kidney lipid levels. Kidney lipid network architecture, particularly of networks involving glycerolipids such as triacylglycerols, was substantially disrupted by worsening kidney disease in the db/db eNOS-/- mice compared to the db/db mice, a feature that was reversed with RAS inhibition. This was associated with decreased expression of the stearoyl-CoA desaturases, Scd1 and Scd2, with RAS inhibition. In addition to the known salutary effect of RAS inhibition on DKD progression, our results suggest a previously unrecognized role for RAS inhibition on the kidney triacylglycerol lipid metabolic network. Keywords: Dyslipidemia is a significant risk factor for progression of diabetic kidney disease (DKD). To identify individual lipids and lipid networks that may be involved in DKD progression, we performed untargeted lipidomic analysis of kidney cortex tissue from diabetic db/db and db/db eNOS-/- mice along with non-diabetic littermate controls. A subset of mice were treated with the renin-angiotensin system (RAS) inhibitors, lisinopril and losartan, which improves the DKD phenotype in the db/db eNOS-/- mouse model. Of the three independent variables in this study, diabetes had the largest impact on overall lipid levels in the kidney cortex, while eNOS expression and RAS inhibition had smaller impacts on kidney lipid levels. Kidney lipid network architecture, particularly of networks involving glycerolipids such as triacylglycerols, was substantially disrupted by worsening kidney disease in the db/db eNOS-/- mice compared to the db/db mice, a feature that was reversed with RAS inhibition. This was associated with decreased expression of the stearoyl-CoA desaturases, Scd1 and Scd2, with RAS inhibition. In addition to the known salutary effect of RAS inhibition on DKD progression, our results suggest a previously unrecognized role for RAS inhibition on the kidney triacylglycerol lipid metabolic network.

Dataset Information

Periodontal pathogen induces entero-hepatic metabolic derangements in type 2 diabetic mouse model

Publications

Porphyromonas gingivalis induces entero-hepatic metabolic derangements with alteration of gut microbiota in a type 2 diabetes mouse model.

Similar Datasets

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