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10.1073/pnas.1113811109 http://scihub22266oqcxt.onion/10.1073/pnas.1113811109 C3396482!3396482 !22733750     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=22733750 &cmd=llinks): Failed to open stream: HTTP request failed! 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Loss of insulin-induced activation of TRPM6 magnesium channels results in impaired glucose tolerance during pregnancy |pdf=|usr=}}{{22733750 }} gab.com Text Loss of insulin-induced activation of TRPM6 magnesium channels results in impaired glucose tolerance during pregnancy JO: Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=22733750 #FOAvip Hypomagnesemia affects insulin resistance and is a risk factor for diabetes mellitus type 2 (DM2) and gestational diabetes mellitus (GDM). Two single nucleotide polymorphisms (SNPs) in the epithelial magnesium channel TRPM6 (V(1393)I, K(1584)E) were predicted to confer susceptibility for DM2. Here, we show using patch clamp analysis and total internal reflection fluorescence microscopy, that insulin stimulates TRPM6 activity via a phosphoinositide 3-kinase and Rac1-mediated elevation of cell surface expression of TRPM6. Interestingly, insulin failed to activate the genetic variants TRPM6(V(1393)I) and TRPM6(K(1584)E), which is likely due to the inability of the insulin signaling pathway to phosphorylate TRPM6(T(1391)) and TRPM6(S(1583)). Moreover, by measuring total glycosylated hemoglobin (TGH) in 997 pregnant women as a measure of glucose control, we demonstrate that TRPM6(V(1393)I) and TRPM6(K(1584)E) are associated with higher TGH and confer a higher likelihood of developing GDM. The impaired response of TRPM6(V(1393)I) and TRPM6(K(1584)E) to insulin represents a unique molecular pathway leading to GDM where the defect is located in TRPM6. Twit Text FOAVip Loss of insulin-induced activation of TRPM6 magnesium channels results in impaired glucose tolerance during pregnancy ????Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=22733750 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=22733750 #FOAvip English Wikipedia <ref>{{Cite pmid|22733750 }}</ref> Loss of insulin-induced activation of TRPM6 magnesium channels results in impaired glucose tolerance during pregnancy #MMPMID22733750 Nair AV ; Hocher B ; Verkaart S ; van Zeeland F ; Pfab T ; Slowinski T ; Chen YP ; Schlingmann KP ; Schaller A ; Gallati S ; Bindels RJ ; Konrad M ; Hoenderop JG Proc Natl Acad Sci U S A 2012[Jul]; 109 (28 ): 11324-9 PMID22733750 show ga Hypomagnesemia affects insulin resistance and is a risk factor for diabetes mellitus type 2 (DM2) and gestational diabetes mellitus (GDM). Two single nucleotide polymorphisms (SNPs) in the epithelial magnesium channel TRPM6 (V(1393)I, K(1584)E) were predicted to confer susceptibility for DM2. Here, we show using patch clamp analysis and total internal reflection fluorescence microscopy, that insulin stimulates TRPM6 activity via a phosphoinositide 3-kinase and Rac1-mediated elevation of cell surface expression of TRPM6. Interestingly, insulin failed to activate the genetic variants TRPM6(V(1393)I) and TRPM6(K(1584)E), which is likely due to the inability of the insulin signaling pathway to phosphorylate TRPM6(T(1391)) and TRPM6(S(1583)). Moreover, by measuring total glycosylated hemoglobin (TGH) in 997 pregnant women as a measure of glucose control, we demonstrate that TRPM6(V(1393)I) and TRPM6(K(1584)E) are associated with higher TGH and confer a higher likelihood of developing GDM. The impaired response of TRPM6(V(1393)I) and TRPM6(K(1584)E) to insulin represents a unique molecular pathway leading to GDM where the defect is located in TRPM6. |*Gene Expression Regulation [MESH] |Cell Line [MESH] |Cytoskeleton/metabolism [MESH] |Diabetes, Gestational/*metabolism [MESH] |Female [MESH] |Genetic Variation [MESH] |Genotype [MESH] |Glucose/*metabolism [MESH] |HEK293 Cells [MESH] |Humans [MESH] |Insulin/*metabolism [MESH] |Kidney/metabolism [MESH] |Microscopy, Fluorescence/methods [MESH] |Models, Biological [MESH] |Patch-Clamp Techniques [MESH] |Phosphorylation [MESH] |Pregnancy [MESH] |Signal Transduction [MESH] |Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization/methods [MESH]Loss of insulin-induced activation of TRPM6 magnesium channels results(epmc).pdf DeepDyve Pubget Overpricing