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Endothelin-1 induces lipolysis in 3T3-L1 adipocytes.
- Source :
- American Journal of Physiology: Endocrinology & Metabolism; Jun2005, Vol. 288, pE1146-E1152, 7p, 1 Diagram, 12 Graphs
- Publication Year :
- 2005
-
Abstract
- Endothelin-1(ET-1) affects glucose uptake in adipocytes and may play an important role in adipose physiology. One of the principal functions of adipose tissue is the provision of energy substrate through lipolysis. In the present study, we investigated the effects of ET-1 on lipolysis in 3T3-L1 adipocytes. When glycerol release in the culture medium was measured as an index of lipolysis, the results showed that ET-1 caused a significant increase that was time and dose dependent. With a concentration of 10 nM ET-1, stimulation of glycerol release plateaued after 4 h of exposure. This effect was inhibited by the ET<subscript>A</subscript> receptor antagonist BQ-610 (10 µM) but not by the ET<subscript>B</subscript> receptor antagonist BQ-788 (10 µM). To further explore the underlying mechanisms of ET-1 action, we examined the involvement of the cAMP-dependent protein kinase A-mediated, phospholipase A<subscript>2</subscript> (PLA<subscript>2</subscript>)mediated, protein kinase C (PKC)-mediated, phosphatidylinositol 3 (PI 3)-kinase-mediated, and the mitogen-activated protein kinase (MAPK)-mediated pathways. Inhibition of adenylyl cyclase activation by SQ-22536 (100 µM) did not block ET-1-induced lipolysis. Pretreatment of adipocytes with the PLA<subscript>2</subscript> inhibitor dexamethasone (100 nM), the PKC inhibitor H-7 (6 µM), or the PI 3-kinase inhibitor wortmannin (100 nM) also had no effect. ET-1-induced lipolysis was blocked by inhibition of extracellular signal-regulated kinase (ERK) activation using PD-98059 (75 µM), whereas a p38 MAPK inhibitor (SB-203580; 20 µM) had no effect. Results of Western blot further demonstrated that ET-1 induced ERK phosphorylation. These data show that ET-1 induces lipolysis in 3T3-L1 adipocytes via a pathway that is different from the conventional cAMP-dependent pathway used by isoproterenol and that involves ERK activation. [ABSTRACT FROM AUTHOR]
- Subjects :
- ENDOTHELINS
LIPOLYSIS
ENZYMES
FAT cells
PEPTIDES
VASOCONSTRICTORS
Subjects
Details
- Language :
- English
- ISSN :
- 01931849
- Volume :
- 288
- Database :
- Complementary Index
- Journal :
- American Journal of Physiology: Endocrinology & Metabolism
- Publication Type :
- Academic Journal
- Accession number :
- 17237853
- Full Text :
- https://doi.org/10.1152/ajpendo.00481.2004