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10.1111/dom.12899 http://scihub22266oqcxt.onion/10.1111/dom.12899 C5484992!5484992!28177189     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28177189&cmd=llinks): Failed to open stream: HTTP request failed! 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Acute physiological effects of glucocorticoids on fuel metabolism in humans are permissive but not direct |pdf=|usr=}}{{28177189}} gab.com Text Acute physiological effects of glucocorticoids on fuel metabolism in humans are permissive but not direct JO: Diabetes Obes Metab http://www.kidney.de/pget.php?&tw=1&pmid=28177189 #FOAvip Background and aims: The effects of glucocorticoids on fuel metabolism are complex. Acute glucocorticoid excess promotes lipolysis but chronic glucocorticoid excess causes visceral fat accumulation. We hypothesized that interactions between cortisol and insulin and adrenaline account for these conflicting results. We tested the effect of cortisol on lipolysis and glucose production with and without insulin and adrenaline in humans both in vivo and in vitro. Materials and methods: A total of 20 healthy men were randomized to low and high insulin groups (both n?=?10). Subjects attended on 3 occasions and received low (c. 150?nM), medium (c. 400?nM) or high (c. 1400?nM) cortisol infusion in a randomized crossover design. Deuterated glucose and glycerol were infused intravenously along with a pancreatic clamp (somatostatin with replacement of glucagon, insulin and growth hormone) and adrenaline. Subcutaneous adipose tissue was obtained for analysis. In parallel, the effect of cortisol on lipolysis was tested in paired primary cultures of human subcutaneous and visceral adipocytes. Results: In vivo, high cortisol increased lipolysis only in the presence of high insulin and/or adrenaline but did not alter glucose kinetics. High cortisol increased adipose mRNA levels of ATGL, HSL and CGI?58 and suppressed G0S2. In vitro, high cortisol increased lipolysis in the presence of insulin in subcutaneous, but not visceral, adipocytes. Conclusions: The acute lipolytic effects of cortisol require supraphysiological concentrations, are dependent on insulin and adrenaline and are observed only in subcutaneous adipose tissue. The resistance of visceral adipose tissue to cortisol's lipolytic effects may contribute to the central fat accumulation observed with chronic glucocorticoid excess. Twit Text FOAVip Acute physiological effects of glucocorticoids on fuel metabolism in humans are permissive but not direct ????Diabetes Obes Metab http://www.kidney.de/pget.php?&tw=1&pmid=28177189 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28177189 #FOAvip English Wikipedia <ref>{{Cite pmid|28177189}}</ref> Acute physiological effects of glucocorticoids on fuel metabolism in humans are permissive but not direct #MMPMID28177189 Stimson RH; Anderson AJ; Ramage LE; Macfarlane DP; de Beaux AC; Mole DJ; Andrew R; Walker BR Diabetes Obes Metab 2017[Jun]; 19 (6): 883-91 PMID28177189show ga Background and aims: The effects of glucocorticoids on fuel metabolism are complex. Acute glucocorticoid excess promotes lipolysis but chronic glucocorticoid excess causes visceral fat accumulation. We hypothesized that interactions between cortisol and insulin and adrenaline account for these conflicting results. We tested the effect of cortisol on lipolysis and glucose production with and without insulin and adrenaline in humans both in vivo and in vitro. Materials and methods: A total of 20 healthy men were randomized to low and high insulin groups (both n?=?10). Subjects attended on 3 occasions and received low (c. 150?nM), medium (c. 400?nM) or high (c. 1400?nM) cortisol infusion in a randomized crossover design. Deuterated glucose and glycerol were infused intravenously along with a pancreatic clamp (somatostatin with replacement of glucagon, insulin and growth hormone) and adrenaline. Subcutaneous adipose tissue was obtained for analysis. In parallel, the effect of cortisol on lipolysis was tested in paired primary cultures of human subcutaneous and visceral adipocytes. Results: In vivo, high cortisol increased lipolysis only in the presence of high insulin and/or adrenaline but did not alter glucose kinetics. High cortisol increased adipose mRNA levels of ATGL, HSL and CGI?58 and suppressed G0S2. In vitro, high cortisol increased lipolysis in the presence of insulin in subcutaneous, but not visceral, adipocytes. Conclusions: The acute lipolytic effects of cortisol require supraphysiological concentrations, are dependent on insulin and adrenaline and are observed only in subcutaneous adipose tissue. The resistance of visceral adipose tissue to cortisol's lipolytic effects may contribute to the central fat accumulation observed with chronic glucocorticoid excess. äAcute physiological effects of glucocorticoids on fuel metabolism in h(epmc).pdf DeepDyve Pubget Overpricing