Dietary fructose-related adiposity and glucocorticoid receptor function in visceral adipose tissue of female rats
Апстракт:
Excessive fructose intake coincides with the growing rate of obesity and
metabolic syndrome, with women being more prone to these disorders than
men. Findings that detrimental effects of fructose might be mediated by
glucocorticoid regeneration in adipose tissue only indirectly implicated
glucocorticoid receptor (GR) in the phenomenon. The aim of the present
study was to elucidate whether fructose overconsumption induces
derangements in GR expression and function that might be associated with
fructose-induced adiposity in females.
We examined effects of fructose-enriched diet on GR expression and
function in visceral adipose tissue of female rats. Additionally, we
analyzed the expression of genes involved in glucocorticoid prereceptor
metabolism {[}11 beta-hydroxysteroid dehydrogenase type 1 (11 beta HSD1)
and hexose-6-phosphate dehydrogenase], lipolysis (hormone-sensitive
lipase) and lipogenesis (sterol regulatory element binding protein 1 and
peroxisomal proliferator-activated receptor gamma).
Fructose-fed rats had elevated energy intake that resulted in visceral
adiposity, as indicated by increased visceral adipose tissue mass and
its share in the whole-body weight. GR hormone binding capacity and
affinity, as well as the expression of GR gene at both mRNA and protein
levels were reduced in visceral adipose tissue of the rats on fructose
diet. The glucocorticoid prereceptor metabolism was stimulated, as
evidenced by elevated tissue corticosterone, while the key regulators of
lipolysis and lipogenesis remained unaffected by fructose diet.
The results suggest that the 11 beta HSD1-mediated elevation of
intracellular corticosterone may induce GR downregulation, which may be
associated with failure of GR to stimulate lipolysis in fructose-fed
female rats.