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10.2337/db16-0698 http://scihub22266oqcxt.onion/10.2337/db16-0698 C5079632!5079632!27495220     free     free     free Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Diabetes 2016 ; 65 (11): 3453-63 Nephropedia Template TP {{tp|p=27495220|t=2016. Renal Denervation Reverses Hepatic Insulin Resistance Induced by High-Fat Diet |pdf=|usr=}}{{27495220}} gab.com Text Renal Denervation Reverses Hepatic Insulin Resistance Induced by High-Fat Diet JO: Diabetes http://www.kidney.de/pget.php?&tw=1&pmid=27495220 #FOAvip Activation of the sympathetic nervous system (SNS) constitutes a putative mechanism of obesity-induced insulin resistance. Thus, we hypothesized that inhibiting the SNS by using renal denervation (RDN) will improve insulin sensitivity (SI) in a nonhypertensive obese canine model. SI was measured using euglycemic-hyperinsulinemic clamp (EGC), before (week 0 [w0]) and after 6 weeks of high-fat diet (w6-HFD) feeding and after either RDN (HFD + RDN) or sham surgery (HFD + sham). As expected, HFD induced insulin resistance in the liver (sham 2.5 ± 0.6 vs. 0.7 ± 0.6 × 10?4 dL ? kg?1 ? min?1 ? pmol/L?1 at w0 vs. w6-HFD [P < 0.05], respectively; HFD + RDN 1.6 ± 0.3 vs. 0.5 ± 0.3 × 10?4 dL ? kg?1 ? min?1 ? pmol/L?1 at w0 vs. w6-HFD [P < 0.001], respectively). In sham animals, this insulin resistance persisted, yet RDN completely normalized hepatic SI in HFD-fed animals (1.8 ± 0.3 × 10?4 dL ? kg?1 ? min?1 ? pmol/L?1 at HFD + RDN [P < 0.001] vs. w6-HFD, [P not significant] vs. w0) by reducing hepatic gluconeogenic genes, including G6Pase, PEPCK, and FOXO1. The data suggest that RDN downregulated hepatic gluconeogenesis primarily by upregulating liver X receptor ? through the natriuretic peptide pathway. In conclusion, bilateral RDN completely normalizes hepatic SI in obese canines. These preclinical data implicate a novel mechanistic role for the renal nerves in the regulation of insulin action specifically at the level of the liver and show that the renal nerves constitute a new therapeutic target to counteract insulin resistance. Twit Text FOAVip Renal Denervation Reverses Hepatic Insulin Resistance Induced by High-Fat Diet ????Diabetes http://www.kidney.de/pget.php?&tw=1&pmid=27495220 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27495220 #FOAvip English Wikipedia <ref>{{Cite pmid|27495220}}</ref> Renal Denervation Reverses Hepatic Insulin Resistance Induced by High-Fat Diet #MMPMID27495220 Iyer MS; Bergman RN; Korman JE; Woolcott OO; Kabir M; Victor RG; Clegg DJ; Kolka C Diabetes 2016[Nov]; 65 (11): 3453-63 PMID27495220show ga Activation of the sympathetic nervous system (SNS) constitutes a putative mechanism of obesity-induced insulin resistance. Thus, we hypothesized that inhibiting the SNS by using renal denervation (RDN) will improve insulin sensitivity (SI) in a nonhypertensive obese canine model. SI was measured using euglycemic-hyperinsulinemic clamp (EGC), before (week 0 [w0]) and after 6 weeks of high-fat diet (w6-HFD) feeding and after either RDN (HFD + RDN) or sham surgery (HFD + sham). As expected, HFD induced insulin resistance in the liver (sham 2.5 ± 0.6 vs. 0.7 ± 0.6 × 10?4 dL ? kg?1 ? min?1 ? pmol/L?1 at w0 vs. w6-HFD [P < 0.05], respectively; HFD + RDN 1.6 ± 0.3 vs. 0.5 ± 0.3 × 10?4 dL ? kg?1 ? min?1 ? pmol/L?1 at w0 vs. w6-HFD [P < 0.001], respectively). In sham animals, this insulin resistance persisted, yet RDN completely normalized hepatic SI in HFD-fed animals (1.8 ± 0.3 × 10?4 dL ? kg?1 ? min?1 ? pmol/L?1 at HFD + RDN [P < 0.001] vs. w6-HFD, [P not significant] vs. w0) by reducing hepatic gluconeogenic genes, including G6Pase, PEPCK, and FOXO1. The data suggest that RDN downregulated hepatic gluconeogenesis primarily by upregulating liver X receptor ? through the natriuretic peptide pathway. In conclusion, bilateral RDN completely normalizes hepatic SI in obese canines. These preclinical data implicate a novel mechanistic role for the renal nerves in the regulation of insulin action specifically at the level of the liver and show that the renal nerves constitute a new therapeutic target to counteract insulin resistance. äRenal Denervation Reverses Hepatic Insulin Resistance Induced by High-(epmc).pdf DeepDyve Pubget Overpricing