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10.1113/expphysiol.2014.078766 http://scihub22266oqcxt.onion/10.1113/expphysiol.2014.078766 C4162767!4162767!25085841     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Exp+Physiol 2014 ; 99 (9): 1140-5 Nephropedia Template TP {{tp|p=25085841|t=2014. Intestinal Regulation of Urinary Sodium Excretion and the Pathophysiology of Diabetic Kidney Disease: A Focus on GLP-1 and DPP-4 |pdf=|usr=}}{{25085841}} gab.com Text Intestinal Regulation of Urinary Sodium Excretion and the Pathophysiology of Diabetic Kidney Disease: A Focus on GLP-1 and DPP-4 JO: Exp Physiol http://www.kidney.de/pget.php?&tw=1&pmid=25085841 #FOAvip The tubular hypothesis of glomerular filtration and nephropathy in diabetes is a pathophysiological concept that assigns a critical role to the tubular system, including proximal tubular hyperreabsorption and growth, which is relevant for early glomerular hyperfiltration and later chronic kidney disease. Here we focus on how harnessing the bioactivity of hormones released from the gut may ameliorate the early effects of diabetes on the kidney in part by attenuating proximal tubular hyperreabsorption and growth. The endogenous tone of the glucagon-like peptide 1 (GLP-1)/GLP-1 receptor (GLP-1R) system and its pharmacologic activation are nephroprotective in diabetes independent of changes in blood glucose. This is associated with suppression of increases in kidney weight and glomerular hyperfiltration, which may reflect at least in part its inhibitory effects on tubular hyperreabsorption and growth. Inhibition of dipeptidyl peptidase 4 (DPP-4) is also nephroprotective independent of changes in blood glucose and involves GLP-1/GLP-1R dependent and independent mechanisms. The GLP-1R agonist exendin-4 induces natriuresis via activation of the GLP-1R. In contrast, DPP4 inhibition, which albeit increases circulating GLP-1, drives a GLP-1R independent natriuretic response implying a role for other DPP-4 substrates. The extent to which the intrarenal DPP-4/GLP-1 receptor system contributes to all these changes remains to be established as does the direct impact of the system on renal inflammation. Twit Text FOAVip Intestinal Regulation of Urinary Sodium Excretion and the Pathophysiology of Diabetic Kidney Disease: A Focus on GLP-1 and DPP-4 ????Exp Physiol http://www.kidney.de/pget.php?&tw=1&pmid=25085841 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25085841 #FOAvip English Wikipedia <ref>{{Cite pmid|25085841}}</ref> Intestinal Regulation of Urinary Sodium Excretion and the Pathophysiology of Diabetic Kidney Disease: A Focus on GLP-1 and DPP-4 #MMPMID25085841 Vallon V; Docherty NG Exp Physiol 2014[Sep]; 99 (9): 1140-5 PMID25085841show ga The tubular hypothesis of glomerular filtration and nephropathy in diabetes is a pathophysiological concept that assigns a critical role to the tubular system, including proximal tubular hyperreabsorption and growth, which is relevant for early glomerular hyperfiltration and later chronic kidney disease. Here we focus on how harnessing the bioactivity of hormones released from the gut may ameliorate the early effects of diabetes on the kidney in part by attenuating proximal tubular hyperreabsorption and growth. The endogenous tone of the glucagon-like peptide 1 (GLP-1)/GLP-1 receptor (GLP-1R) system and its pharmacologic activation are nephroprotective in diabetes independent of changes in blood glucose. This is associated with suppression of increases in kidney weight and glomerular hyperfiltration, which may reflect at least in part its inhibitory effects on tubular hyperreabsorption and growth. Inhibition of dipeptidyl peptidase 4 (DPP-4) is also nephroprotective independent of changes in blood glucose and involves GLP-1/GLP-1R dependent and independent mechanisms. The GLP-1R agonist exendin-4 induces natriuresis via activation of the GLP-1R. In contrast, DPP4 inhibition, which albeit increases circulating GLP-1, drives a GLP-1R independent natriuretic response implying a role for other DPP-4 substrates. The extent to which the intrarenal DPP-4/GLP-1 receptor system contributes to all these changes remains to be established as does the direct impact of the system on renal inflammation. äIntestinal Regulation of Urinary Sodium Excretion and the Pathophysiol(epmc).pdf DeepDyve Pubget Overpricing