DIETARY ENERGY RESTRICTION IN THE SENCAR MOUSE - ELEVATION OF GLUCOCORTICOID HORMONE LEVELS BUT NO CHANGE IN DISTRIBUTION OF GLUCOCORTICOIDRECEPTOR IN EPIDERMAL-CELLS
Al. Yaktine et al., DIETARY ENERGY RESTRICTION IN THE SENCAR MOUSE - ELEVATION OF GLUCOCORTICOID HORMONE LEVELS BUT NO CHANGE IN DISTRIBUTION OF GLUCOCORTICOIDRECEPTOR IN EPIDERMAL-CELLS, Molecular carcinogenesis, 21(1), 1998, pp. 62-69
The purpose of this study was to demonstrate that dietary energy restr
iction elevates plasma glucocorticoid hormone (GCH) levels while maint
aining a circadian profile. Furthermore, we indirectly measured the ef
fect of energy restriction on receptor activation in epidermis by dete
rmining the cellular localization of receptor protein in control-fed a
nd energy-restricted (ER) mice. SENCAR mice were maintained on an ad l
ibitum control diet or an ER diet that provided 60% of the total energ
y consumed by control-fed mice. Plasma corticosterone levels were dete
rmined by radioimmunoassay. Glucocorticoid receptor (CR) protein level
s in epidermal lysates were measured by western blotting. Electron mic
roscopy was used to identify gold-conjugated immunoreactive GR in epid
ermal cells of the skin in control and ER mice. Plasma corticosterone
levels in ER mice were significantly increased 10 times over the level
s in control mice at 0700 h, significantly increased two times over co
ntrol levels at 1600 h, and not different from controls at 2300 h in t
he circadian cycle. The total amount of epidermal GR protein in ER mic
e was 140% (95% confidence interval, 104-169%) of that in controls at
the early time point, not different at the midpoint, and 60% (95% conf
idence interval, 48-79%) of that in controls at the late time point. T
he distribution of gold-conjugated GR in the cytoplasmic and nuclear c
ompartments of epidermal cells was similar in control and ER mice. Thu
s, we showed that dietary ER increased the level of plasma GCH without
abolishing diurnal variation. However, an increase in ligand activati
on in epidermal cells, as indicated by nuclear localization of GR prot
ein, was not supported by the results of this study. (C) 1998 Wiley-Li
ss, Inc.