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10.1371/journal.pone.0200249 http://scihub22266oqcxt.onion/10.1371/journal.pone.0200249 C6034861!6034861 !29979777     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29979777 &cmd=llinks): Failed to open stream: HTTP request failed! 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Linagliptin unmasks specific antioxidant pathways protective against albuminuria and kidney hypertrophy in a mouse model of diabetes |pdf=|usr=}}{{29979777 }} gab.com Text Linagliptin unmasks specific antioxidant pathways protective against albuminuria and kidney hypertrophy in a mouse model of diabetes JO: PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=29979777 #FOAvip BACKGROUND: Dipeptidyl peptidase-4 (DPP-4) inhibitors may have protective effects on diabetic kidney disease (DKD) via specific antioxidant pathways. The DPP-4 inhibitor, linagliptin, was evaluated with the hypothesis that DPP-4 inhibition would ameliorate the development of DKD in a glucose-independent manner by altering specific antioxidant function. METHODS: DBA/2J mice (a well-characterized model of DKD) and glucose 6-phosphate dehydrogenase (G6PD) deficient mice (a model of impaired antioxidant function) were evaluated. Diabetes was induced by streptozotocin. Mice were divided into: diabetic (DM), diabetic+linagliptin (DM+Lina), and non-diabetic control and treated for 12 weeks. RESULTS: In DBA/2J mice, there was no difference in body weight and blood glucose between DM and DM+Lina groups. Linagliptin ameliorated albuminuria and kidney hypertrophy in DM DBA/2J mice and specifically increased the mRNA and protein levels for the antioxidants catalase and MnSOD. In G6PD deficient mice, however, increases in these mRNA levels did not occur and linagliptin renoprotection was not observed. Linagliptin also ameliorated histological trends toward mesangial expansion in wild-type mice but not in G6PD deficient mice. CONCLUSIONS: Linagliptin renoprotection involved glucose-independent but antioxidant-enzyme-system-dependent increases in transcription (not just increased protein levels) of antioxidant proteins in wild-type mice. These studies demonstrate that an intact antioxidant system, in particular including transcription of catalase and MnSOD, is required for the renoprotective effects of linagliptin. Twit Text FOAVip Linagliptin unmasks specific antioxidant pathways protective against albuminuria and kidney hypertrophy in a mouse model of diabetes ????PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=29979777 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29979777 #FOAvip English Wikipedia <ref>{{Cite pmid|29979777 }}</ref> Linagliptin unmasks specific antioxidant pathways protective against albuminuria and kidney hypertrophy in a mouse model of diabetes #MMPMID29979777 Spencer NY ; Yang Z ; Sullivan JC ; Klein T ; Stanton RC PLoS One 2018[]; 13 (7 ): e0200249 PMID29979777 show ga BACKGROUND: Dipeptidyl peptidase-4 (DPP-4) inhibitors may have protective effects on diabetic kidney disease (DKD) via specific antioxidant pathways. The DPP-4 inhibitor, linagliptin, was evaluated with the hypothesis that DPP-4 inhibition would ameliorate the development of DKD in a glucose-independent manner by altering specific antioxidant function. METHODS: DBA/2J mice (a well-characterized model of DKD) and glucose 6-phosphate dehydrogenase (G6PD) deficient mice (a model of impaired antioxidant function) were evaluated. Diabetes was induced by streptozotocin. Mice were divided into: diabetic (DM), diabetic+linagliptin (DM+Lina), and non-diabetic control and treated for 12 weeks. RESULTS: In DBA/2J mice, there was no difference in body weight and blood glucose between DM and DM+Lina groups. Linagliptin ameliorated albuminuria and kidney hypertrophy in DM DBA/2J mice and specifically increased the mRNA and protein levels for the antioxidants catalase and MnSOD. In G6PD deficient mice, however, increases in these mRNA levels did not occur and linagliptin renoprotection was not observed. Linagliptin also ameliorated histological trends toward mesangial expansion in wild-type mice but not in G6PD deficient mice. CONCLUSIONS: Linagliptin renoprotection involved glucose-independent but antioxidant-enzyme-system-dependent increases in transcription (not just increased protein levels) of antioxidant proteins in wild-type mice. These studies demonstrate that an intact antioxidant system, in particular including transcription of catalase and MnSOD, is required for the renoprotective effects of linagliptin. |Albuminuria/metabolism/pathology/*prevention & control [MESH] |Animals [MESH] |Blood Glucose/drug effects [MESH] |Blood Pressure/drug effects [MESH] |Body Weight/drug effects [MESH] |Catalase/blood [MESH] |Diabetes Mellitus, Experimental/*drug therapy/metabolism/pathology [MESH] |Diabetic Nephropathies/metabolism/pathology/*prevention & control [MESH] |Dipeptidyl-Peptidase IV Inhibitors/*pharmacology/therapeutic use [MESH] |Glucosephosphate Dehydrogenase/genetics/metabolism [MESH] |Hypoglycemic Agents/*pharmacology/therapeutic use [MESH] |Kidney/drug effects/metabolism/pathology [MESH] |Linagliptin/*pharmacology/therapeutic use [MESH] |Mice [MESH] |Mice, Knockout [MESH] |Oxidative Stress/*drug effects [MESH]Linagliptin unmasks specific antioxidant pathways protective against a(epmc).pdf DeepDyve Pubget Overpricing