Jn. Fain et Sw. Bahouth, Hormonal regulation of 18S RNA, leptin mRNA, and leptin release in adipocytes from hypothyroid rats, METABOLISM, 47(12), 1998, pp. 1455-1461
The present studies were designed to examine the regulation of leptin relea
se in primary cultures of adipocytes from fed hypothyroid rats incubated wi
th hormones for 24 hours. Leptin release was increased in the presence of d
examethasone. while the decrease in leptin mRNA content over a 24-hour incu
bation was reduced by dexamethasone. Dexamethasone did not affect the glyce
raldehyde-3-phosphate dehydrogenase (GAPDH) mRNA or 18S RNA content of adip
ocytes. Insulin increased leptin release by adipocytes in both the absence
and presence of dexamethasone. Although insulin also prevented the loss of
leptin mRNA. this effect was less than that observed for GAPDH mRNA or 18S
RNA content. In isolated adipocytes. the loss of almost half the 18S RNA co
ntent over a 24-hour incubation was prevented in the presence of insulin bu
t not oxytocin or epidermal growth factor (EGF). The specific beta(3) catec
holamine agonist CI 316,243 inhibited the effects of dexamethasone on lepti
n release and leptin mRNA accumulation, as did EGF, without affecting 18S R
NA content. Oxytocin inhibited the increase in leptin release due to dexame
thasone without affecting leptin mRNA levels. These data indicate that alth
ough dexamethasone and insulin are positive regulators of leptin release, o
nly dexamethasone specifically prevented the loss of leptin mRNA in culture
d rat adipocytes. In contrast, insulin, but not dexamethasone. prevented th
e marked loss in 185 RNA observed over a 24-hour incubation of rat adipocyt
es. Copyright (C) 1998 by W.B. Saunders Company.