GLP-1/GLP-1R Signaling in Regulation of Adipocyte Differentiation and Lipogenesis.
Cell Physiol Biochem
; 42(3): 1165-1176, 2017.
Article
en En
| MEDLINE
| ID: mdl-28668964
ABSTRACT
BACKGROUND/AIMS:
The aim of this study was to determine the direct role of liraglutide (LG) in adipogenesis and lipid metabolism.METHODS:
Lipid accumulation was evaluated by oil red O staining, quantitative real-time PCR (qPCR) was performed to determine glucagon-like peptide 1 receptor (GLP-1R), fatty acid synthase (FASN) and adipose triglyceride lipase (ATGL) expression in 3T3-L1 preadipocytes, differentiated adipocytes and in adipose tissues from mice. The effects of LG on 3T3-L1 adipogenesis and lipid metabolism were analyzed with qPCR, Western Blotting, oil red O staining, immunohistochemistry (IHC) and immunofluorescence (IF). All measurements were performed at least three times.RESULTS:
LG increased the expression of differentiation marker genes and lipid accumulation during preadipocyte differentiation. In differentiated adipocytes, LG decreased FASN expression, and simultaneously led to CREB phosphorylation and ERK1/2 activation which were abolished by a GLP-1R antagonist, exendin (9-39). LG induced-FASN down-regulation was partially reversed by PKA and ERK1/2 inhibitors. Consistent with above in vitro findings, LG treatment significantly reduced FASN expression in visceral adipose tissues of ob/ob mice, and reduced body weight gain.CONCLUSION:
LG promotes preadipocytes differentiation, and inhibits FASN expression in adipocytes. LG induced down-regulation of FASN is at least partially mediated by PKA and MAPK signaling pathways.Palabras clave
Texto completo:
1
Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Adipocitos
/
Péptido 1 Similar al Glucagón
/
Adipogénesis
/
Lipogénesis
/
Liraglutida
/
Receptor del Péptido 1 Similar al Glucagón
/
Hipoglucemiantes
Límite:
Animals
Idioma:
En
Revista:
Cell Physiol Biochem
Asunto de la revista:
BIOQUIMICA
/
FARMACOLOGIA
Año:
2017
Tipo del documento:
Article
País de afiliación:
China