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10.1172/jci.insight.91809 http://scihub22266oqcxt.onion/10.1172/jci.insight.91809 C5396514!5396514!28422755     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       JCI+Insight ä ; 2 (8): ä Nephropedia Template TP {{tp|p=28422755|t=ä. ?-Klotho deficiency protects against obesity through a crosstalk between liver, microbiota, and brown adipose tissue |pdf=|usr=}}{{28422755}} gab.com Text -Klotho deficiency protects against obesity through a crosstalk between liver, microbiota, and brown adipose tissue JO: JCI Insight http://www.kidney.de/pget.php?&tw=1&pmid=28422755 #FOAvip ?-Klotho (encoded by Klb) is the obligate coreceptor mediating FGF21 and FGF15/19 signaling. Klb?/? mice are refractory to beneficial action of pharmacological FGF21 treatment including stimulation of glucose utilization and thermogenesis. Here, we investigated the energy homeostasis in Klb?/? mice on high-fat diet in order to better understand the consequences of abrogating both endogenous FGF15/19 and FGF21 signaling during caloric overload. Surprisingly, Klb?/? mice are resistant to diet-induced obesity (DIO) owing to enhanced energy expenditure and BAT activity. Klb?/? mice exhibited not only an increase but also a shift in bile acid (BA) composition featured by activation of the classical (neutral) BA synthesis pathway at the expense of the alternative (acidic) pathway. High hepatic production of cholic acid (CA) results in a large excess of microbiota-derived deoxycholic acid (DCA). DCA is specifically responsible for activating the TGR5 receptor that stimulates BAT thermogenic activity. In fact, combined gene deletion of Klb and Tgr5 or antibiotic treatment abrogating bacterial conversion of CA into DCA both abolish DIO resistance in Klb?/? mice. These results suggested that DIO resistance in Klb?/? mice is caused by high levels of DCA, signaling through the TGR5 receptor. These data also demonstrated that gut microbiota can regulate host thermogenesis via conversion of primary into secondary BA. Pharmacologic or nutritional approaches to selectively modulate BA composition may be a promising target for treating metabolic disorders. Twit Text FOAVip -Klotho deficiency protects against obesity through a crosstalk between liver, microbiota, and brown adipose tissue ????JCI Insight http://www.kidney.de/pget.php?&tw=1&pmid=28422755 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28422755 #FOAvip English Wikipedia <ref>{{Cite pmid|28422755}}</ref> ?-Klotho deficiency protects against obesity through a crosstalk between liver, microbiota, and brown adipose tissue #MMPMID28422755 Somm E; Henry H; Bruce SJ; Aeby S; Rosikiewicz M; Sykiotis GP; Asrih M; Jornayvaz FR; Denechaud PD; Albrecht U; Mohammadi M; Dwyer A; Acierno JS; Schoonjans K; Fajas L; Greub G; Pitteloud N JCI Insight ä[]; 2 (8): ä PMID28422755show ga ?-Klotho (encoded by Klb) is the obligate coreceptor mediating FGF21 and FGF15/19 signaling. Klb?/? mice are refractory to beneficial action of pharmacological FGF21 treatment including stimulation of glucose utilization and thermogenesis. Here, we investigated the energy homeostasis in Klb?/? mice on high-fat diet in order to better understand the consequences of abrogating both endogenous FGF15/19 and FGF21 signaling during caloric overload. Surprisingly, Klb?/? mice are resistant to diet-induced obesity (DIO) owing to enhanced energy expenditure and BAT activity. Klb?/? mice exhibited not only an increase but also a shift in bile acid (BA) composition featured by activation of the classical (neutral) BA synthesis pathway at the expense of the alternative (acidic) pathway. High hepatic production of cholic acid (CA) results in a large excess of microbiota-derived deoxycholic acid (DCA). DCA is specifically responsible for activating the TGR5 receptor that stimulates BAT thermogenic activity. In fact, combined gene deletion of Klb and Tgr5 or antibiotic treatment abrogating bacterial conversion of CA into DCA both abolish DIO resistance in Klb?/? mice. These results suggested that DIO resistance in Klb?/? mice is caused by high levels of DCA, signaling through the TGR5 receptor. These data also demonstrated that gut microbiota can regulate host thermogenesis via conversion of primary into secondary BA. Pharmacologic or nutritional approaches to selectively modulate BA composition may be a promising target for treating metabolic disorders. ä?-Klotho deficiency protects against obesity through a crosstalk betwe(epmc).pdf DeepDyve Pubget Overpricing