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10.1038/labinvest.2015.129 http://scihub22266oqcxt.onion/10.1038/labinvest.2015.129 C4695279!4695279!26552046     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       Lab+Invest 2016 ; 96 (1): 98-111 Nephropedia Template TP {{tp|p=26552046|t=2016. Regulation of intestinal SGLT1 by catestatin in hyperleptinemic type 2 diabetic mice |pdf=|usr=}}{{26552046}} gab.com Text Regulation of intestinal SGLT1 by catestatin in hyperleptinemic type 2 diabetic mice JO: Lab Invest http://www.kidney.de/pget.php?&tw=1&pmid=26552046 #FOAvip The small intestine is the major site for nutrient absorption, which is critical in maintenance of euglycemia. Leptin, a key hormone involved in energy homeostasis, directly affects nutrient transport across the intestinal epithelium. Catestatin (CST), a 21-amino acid peptide derived from proprotein chromogranin A, has been shown to modulate leptin signaling. Therefore, we reasoned that leptin and CST could modulate intestinal Na+-glucose transporter 1 (SGLT1) expression in the context of obesity and diabetes. We found that hyperleptinemic db/db mice exhibit increased mucosal mass, associated with an enhanced proliferative response and decreased apoptosis in intestinal crypts, a finding absent in leptin deficient ob/ob mice. Intestinal SGLT1 abundance was significantly decreased in hyperleptinemic, but not leptin-deficient mice, indicating leptin regulation of SGLT1 expression. Phlorizin, a SGLT1/2 inhibitor, was without effect in an oral glucose tolerance test in db/db mice. The alterations in architecture and SGLT1 abundance were not accompanied by changes in the localization of intestinal alkaline phosphatase, indicating intact differentiation. Treatment of db/db mice with CST restored intestinal SGLT1 abundance and intestinal turnover, suggesting a cross-talk between leptin and CST, without affecting plasma leptin levels. Consistent with this hypothesis, we identified structural homology between CST and the AB-loop of leptin and protein-protein docking revealed binding of CST and leptin with the Ig-like binding site III of the leptin receptor. In summary, downregulation of SGLT1 in an obese type 2 diabetic mouse model with hyperleptinemia is presumably mediated via the short form of the leptin receptor and reduces overt hyperglycemia. Twit Text FOAVip Regulation of intestinal SGLT1 by catestatin in hyperleptinemic type 2 diabetic mice ????Lab Invest http://www.kidney.de/pget.php?&tw=1&pmid=26552046 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26552046 #FOAvip English Wikipedia <ref>{{Cite pmid|26552046}}</ref> Regulation of intestinal SGLT1 by catestatin in hyperleptinemic type 2 diabetic mice #MMPMID26552046 Rieg JAD; Chirasani VR; Koepsell H; Senapati S; Mahata SK; Rieg T Lab Invest 2016[Jan]; 96 (1): 98-111 PMID26552046show ga The small intestine is the major site for nutrient absorption, which is critical in maintenance of euglycemia. Leptin, a key hormone involved in energy homeostasis, directly affects nutrient transport across the intestinal epithelium. Catestatin (CST), a 21-amino acid peptide derived from proprotein chromogranin A, has been shown to modulate leptin signaling. Therefore, we reasoned that leptin and CST could modulate intestinal Na+-glucose transporter 1 (SGLT1) expression in the context of obesity and diabetes. We found that hyperleptinemic db/db mice exhibit increased mucosal mass, associated with an enhanced proliferative response and decreased apoptosis in intestinal crypts, a finding absent in leptin deficient ob/ob mice. Intestinal SGLT1 abundance was significantly decreased in hyperleptinemic, but not leptin-deficient mice, indicating leptin regulation of SGLT1 expression. Phlorizin, a SGLT1/2 inhibitor, was without effect in an oral glucose tolerance test in db/db mice. The alterations in architecture and SGLT1 abundance were not accompanied by changes in the localization of intestinal alkaline phosphatase, indicating intact differentiation. Treatment of db/db mice with CST restored intestinal SGLT1 abundance and intestinal turnover, suggesting a cross-talk between leptin and CST, without affecting plasma leptin levels. Consistent with this hypothesis, we identified structural homology between CST and the AB-loop of leptin and protein-protein docking revealed binding of CST and leptin with the Ig-like binding site III of the leptin receptor. In summary, downregulation of SGLT1 in an obese type 2 diabetic mouse model with hyperleptinemia is presumably mediated via the short form of the leptin receptor and reduces overt hyperglycemia. äRegulation of intestinal SGLT1 by catestatin in hyperleptinemic type 2(epmc).pdf DeepDyve Pubget Overpricing