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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Diabetes+Obes+Metab
2017 ; 19
(6
): 883-891
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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
): 883-891
PMID28177189
show 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.