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10.1155/2018/5697970 http://scihub22266oqcxt.onion/10.1155/2018/5697970 C5996472!5996472 !30003110     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=30003110 &cmd=llinks): Failed to open stream: HTTP request failed! 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The Antidiabetic Agent Sodium Tungstate Induces Abnormal Glycogen Accumulation in Renal Proximal Tubules from Diabetic IRS2-Knockout Mice |pdf=|usr=}}{{30003110 }} gab.com Text The Antidiabetic Agent Sodium Tungstate Induces Abnormal Glycogen Accumulation in Renal Proximal Tubules from Diabetic IRS2-Knockout Mice JO: J Diabetes Res http://www.kidney.de/pget.php?&tw=1&pmid=30003110 #FOAvip The kidney is an insulin-sensitive organ involved in glucose homeostasis. One major effect of insulin is to induce glycogen storage in the liver and muscle. However, no significant glycogen stores are detected in normal kidneys, but diabetic subjects present a characteristic renal histopathological feature resulting from extensive glycogen deposition mostly in nonproximal tubules. The mechanism of renal glycogen accumulation is yet poorly understood. Here, we studied in situ glycogen accumulation in the kidney from diabetic IRS2-knockout mice and the effect of the insulin-mimetic agent sodium tungstate (NaW). IRS2-knockout mice displayed hyperglycemia and hyperinsulinemia. NaW only normalized glycemia. There was no evident morphological difference between kidneys from untreated wild-type (WT), NaW-treated WT, and untreated IRS2-knockout mice. However, NaW-treated IRS2-knockout mice showed tubular alterations resembling clear cells in the cortex, but not in the outer medulla, that were correlated with glycogen accumulation. Immunohistochemical detection of the gluconeogenic enzyme phosphoenolpyruvate carboxykinase, mostly expressed by renal proximal tubules, showed that altered tubules were of proximal origin. Our preliminary study suggests that IRS2 differentially regulates glycogen accumulation in renal tubules and that NaW treatment in the context of IRS2 ablation induces abnormal glycogen accumulation in cortical proximal tubules. Twit Text FOAVip The Antidiabetic Agent Sodium Tungstate Induces Abnormal Glycogen Accumulation in Renal Proximal Tubules from Diabetic IRS2-Knockout Mice ????J Diabetes Res http://www.kidney.de/pget.php?&tw=1&pmid=30003110 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=30003110 #FOAvip English Wikipedia <ref>{{Cite pmid|30003110 }}</ref> The Antidiabetic Agent Sodium Tungstate Induces Abnormal Glycogen Accumulation in Renal Proximal Tubules from Diabetic IRS2-Knockout Mice #MMPMID30003110 Bertinat R ; Westermeier F ; Silva P ; Gatica R ; Oliveira JM ; Nualart F ; Gomis R ; Yáñez AJ J Diabetes Res 2018[]; 2018 (ä): 5697970 PMID30003110 show ga The kidney is an insulin-sensitive organ involved in glucose homeostasis. One major effect of insulin is to induce glycogen storage in the liver and muscle. However, no significant glycogen stores are detected in normal kidneys, but diabetic subjects present a characteristic renal histopathological feature resulting from extensive glycogen deposition mostly in nonproximal tubules. The mechanism of renal glycogen accumulation is yet poorly understood. Here, we studied in situ glycogen accumulation in the kidney from diabetic IRS2-knockout mice and the effect of the insulin-mimetic agent sodium tungstate (NaW). IRS2-knockout mice displayed hyperglycemia and hyperinsulinemia. NaW only normalized glycemia. There was no evident morphological difference between kidneys from untreated wild-type (WT), NaW-treated WT, and untreated IRS2-knockout mice. However, NaW-treated IRS2-knockout mice showed tubular alterations resembling clear cells in the cortex, but not in the outer medulla, that were correlated with glycogen accumulation. Immunohistochemical detection of the gluconeogenic enzyme phosphoenolpyruvate carboxykinase, mostly expressed by renal proximal tubules, showed that altered tubules were of proximal origin. Our preliminary study suggests that IRS2 differentially regulates glycogen accumulation in renal tubules and that NaW treatment in the context of IRS2 ablation induces abnormal glycogen accumulation in cortical proximal tubules. |Animals [MESH] |Diabetes Mellitus, Experimental/metabolism/*pathology [MESH] |Diabetic Nephropathies/metabolism [MESH] |Glycogen/*metabolism [MESH] |Hypoglycemic Agents/*pharmacology [MESH] |Insulin Receptor Substrate Proteins/genetics [MESH] |Insulin Resistance [MESH] |Insulin/metabolism [MESH] |Kidney Tubules, Proximal/drug effects/*metabolism [MESH] |Kidney/metabolism [MESH] |Male [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Mice, Knockout [MESH] |Phosphoenolpyruvate Carboxykinase (ATP)/metabolism [MESH] |Signal Transduction/drug effects [MESH]The Antidiabetic Agent Sodium Tungstate Induces Abnormal Glycogen Accu(epmc).pdf DeepDyve Pubget Overpricing