Characterization of murine melanocortin receptors mediating adipocyte lipolysis and examination of signalling pathways involved
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Characterization of murine melanocortin receptors mediating adipocyte lipolysis and examination of signalling pathways involved. / Møller, Cathrine Laustrup; Raun, Kirsten; Jacobsen, Marianne Lambert; Pedersen, Thomas Åskov; Holst, Birgitte; Conde-Frieboes, Kilian W; Wulff, Birgitte Schjellerup.
In: Molecular and Cellular Endocrinology, Vol. 341, No. 1-2, 20.07.2011, p. 9-17.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Characterization of murine melanocortin receptors mediating adipocyte lipolysis and examination of signalling pathways involved
AU - Møller, Cathrine Laustrup
AU - Raun, Kirsten
AU - Jacobsen, Marianne Lambert
AU - Pedersen, Thomas Åskov
AU - Holst, Birgitte
AU - Conde-Frieboes, Kilian W
AU - Wulff, Birgitte Schjellerup
N1 - Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.
PY - 2011/7/20
Y1 - 2011/7/20
N2 - The melanocortin receptors (MCRs) belong to the G-protein coupled receptors (family A). So far, 5 different subtypes have been described (MC1R-MC5R) and of these MC2R and MC5R have been proposed to act directly in adipocytes and regulate lipolysis in rodents. Using ACTH and a-melanocyte stimulating hormone (a-MSH) generated from proopiomelanocortin (POMC), as well as synthetic MSH analogues to stimulate lipolysis in murine 3T3-L1 adipocytes it is shown that MC2R and MC5R are lipolytic mediators in differentiated 3T3-L1 adipocytes. Involvement of cAMP, phosphorylated extracellular signal-regulated kinase (ERK) 1/2, protein kinase B (PKB), adenosine 5' monophosphate activated protein kinase (AMPK) and Jun-amino-terminal kinase (JNK) in MCR mediated lipolysis were studied. Interestingly, results obtained in 3T3-L1 cells suggest that lipolysis stimulated by a-MSH, NDP-a-MSH, MT-II, SHU9119 and PG-901 is mediated through MC5R in a cAMP independent manner. Finally, we identify essential differences in MCR mediated lipolysis when using 3T3-L1 cells compared to primary adipocytes.
AB - The melanocortin receptors (MCRs) belong to the G-protein coupled receptors (family A). So far, 5 different subtypes have been described (MC1R-MC5R) and of these MC2R and MC5R have been proposed to act directly in adipocytes and regulate lipolysis in rodents. Using ACTH and a-melanocyte stimulating hormone (a-MSH) generated from proopiomelanocortin (POMC), as well as synthetic MSH analogues to stimulate lipolysis in murine 3T3-L1 adipocytes it is shown that MC2R and MC5R are lipolytic mediators in differentiated 3T3-L1 adipocytes. Involvement of cAMP, phosphorylated extracellular signal-regulated kinase (ERK) 1/2, protein kinase B (PKB), adenosine 5' monophosphate activated protein kinase (AMPK) and Jun-amino-terminal kinase (JNK) in MCR mediated lipolysis were studied. Interestingly, results obtained in 3T3-L1 cells suggest that lipolysis stimulated by a-MSH, NDP-a-MSH, MT-II, SHU9119 and PG-901 is mediated through MC5R in a cAMP independent manner. Finally, we identify essential differences in MCR mediated lipolysis when using 3T3-L1 cells compared to primary adipocytes.
U2 - 10.1016/j.mce.2011.03.010
DO - 10.1016/j.mce.2011.03.010
M3 - Journal article
C2 - 21616121
VL - 341
SP - 9
EP - 17
JO - Molecular and Cellular Endocrinology
JF - Molecular and Cellular Endocrinology
SN - 0303-7207
IS - 1-2
ER -
ID: 33802580