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10.1074/jbc.M115.707448 http://scihub22266oqcxt.onion/10.1074/jbc.M115.707448 C4933223!4933223!27137930     free     free     free Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Biol+Chem 2016 ; 291 (25): 13063-75 Nephropedia Template TP {{tp|p=27137930|t=2016. The Amplifying Pathway of the ?-Cell Contributes to Diet-induced Obesity* |pdf=|usr=}}{{27137930}} gab.com Text The Amplifying Pathway of the -Cell Contributes to Diet-induced Obesity* JO: J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=27137930 #FOAvip Efficient energy storage in adipose tissues requires optimal function of the insulin-producing ?-cell, whereas its dysfunction promotes diabetes. The associated paradox related to ?-cell efficiency is that excessive accumulation of fat in adipose tissue predisposes for type 2 diabetes. Insulin exocytosis is regulated by intracellular metabolic signal transduction, with glutamate dehydrogenase playing a key role in the amplification of the secretory response. Here, we used mice with ?-cell-selective glutamate dehydrogenase deletion (?Glud1?/?), lacking an amplifying pathway of insulin secretion. As opposed to control mice, ?Glud1?/? animals fed a high calorie diet maintained glucose tolerance and did not develop diet-induced obesity. Islets of ?Glud1?/? mice did not increase their secretory response upon high calorie feeding, as did islets of control mice. Inhibited adipose tissue expansion observed in knock-out mice correlated with lower expression of genes responsible for adipogenesis. Rather than being efficiently stored, lipids were consumed at a higher rate in ?Glud1?/? mice compared with controls, in particular during food intake periods. These results show that reduced ?-cell function prior to high calorie feeding prevented diet-induced obesity. Twit Text FOAVip The Amplifying Pathway of the -Cell Contributes to Diet-induced Obesity* ????J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=27137930 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27137930 #FOAvip English Wikipedia <ref>{{Cite pmid|27137930}}</ref> The Amplifying Pathway of the ?-Cell Contributes to Diet-induced Obesity* #MMPMID27137930 Vetterli L; Carobbio S; Frigerio F; Karaca M; Maechler P J Biol Chem 2016[Jun]; 291 (25): 13063-75 PMID27137930show ga Efficient energy storage in adipose tissues requires optimal function of the insulin-producing ?-cell, whereas its dysfunction promotes diabetes. The associated paradox related to ?-cell efficiency is that excessive accumulation of fat in adipose tissue predisposes for type 2 diabetes. Insulin exocytosis is regulated by intracellular metabolic signal transduction, with glutamate dehydrogenase playing a key role in the amplification of the secretory response. Here, we used mice with ?-cell-selective glutamate dehydrogenase deletion (?Glud1?/?), lacking an amplifying pathway of insulin secretion. As opposed to control mice, ?Glud1?/? animals fed a high calorie diet maintained glucose tolerance and did not develop diet-induced obesity. Islets of ?Glud1?/? mice did not increase their secretory response upon high calorie feeding, as did islets of control mice. Inhibited adipose tissue expansion observed in knock-out mice correlated with lower expression of genes responsible for adipogenesis. Rather than being efficiently stored, lipids were consumed at a higher rate in ?Glud1?/? mice compared with controls, in particular during food intake periods. These results show that reduced ?-cell function prior to high calorie feeding prevented diet-induced obesity. äThe Amplifying Pathway of the ?-Cell Contributes to Diet-induced Obesi(epmc).pdf DeepDyve Pubget Overpricing