Abstract:
Abstract—One of the tissues taking the biggest part in the
pathogenesis of obesity is adipose tissue mainly formed by white
fat cells. Recently, the processes adipogenesis become a
treatment target for obesity. One of the pathway that allegedly
participated in the process of adipogenesis is activated via
CREB. The upstream pathway is by means of protein of
mammalian targets of rapamycin (mTOR). This study was
aimed to determine the role of CREB in adipogenesis through
the activation of p70S6K1 by mTORC1.
This was an experimental study. Subjects were primary
cultured preadipocytes taken from visceral fat of white rats
(Rattus norvegicus). Cell cultures were classified into 4 groups:
(K) Control of adipogenesis: without rapamycin and RNAi
CREB, (A): was given rapamycin 10 nM, (B): was given RNAi
CREB 100 nM, (C): was given rapamycin 10 nM and RNAi
CREB 100 nM. p70S6K1, CREB activation, and expression of
C/EBPδ measured on day 2, 4, and 6, and the morphology of
adipocytes on day 6. Data were analyzed with Anova test, LSD
test, and Pearson correlation test with 95% confidence level.
The data showed that rapamycin activated p70S6K1 and
caused lower CREB compared with control group during
adipogenesis. These results indicated that adipogenesis was
blocked, which resulted from the inhibition of p70S6K1 and
CREB activation by rapamycin and RNAi CREB. The
inhibition was stronger in rapamycin + RNAi CREB group.
Statistically, there was significant correlation between p70S6K1
and CREB; and between CREB and C/EBPδ.
It was concluded that the role of CREB in adipogenesis
