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Oxytocin attenuates beta oxidation and fatty acid synthesis through CPT1α and FABP4 (605.8)
Author(s) -
Han Jen Lin,
Mersmann Harry,
Shin Torng Ding
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.605.8
Subject(s) - oxytocin , endocrinology , medicine , beta oxidation , chemistry , triglyceride , energy homeostasis , carnitine , lipid metabolism , fatty acid , metabolism , biology , biochemistry , cholesterol , receptor
Oxytocin has a role in regulating body energy homeostasis. It’s demonstrated that central and subcutaneous oxytocin infusions stimulated lipid metabolism both in standard and high fat diet mice and rats. To study the effects of oxytocin on lipid metabolism, we tested series concentrations of oxytocin (0, 10, 33, 100, 150, 333 nM) to 3T3L1 adipocytes for both long (216 hours) and short (24 hours) time periods. Our results showed that short term treatment of 150 nM oxytocin significantly increased triglyceride accumulation, but decreased mRNA expressions of forkhead box protein O1 (FoxO1), carnitine palmitoyltransferase Iα (CPT1α), fatty acid binding protein 4 (FABP4); however, only CPT1α decreased after long term treatment of 150 nM oxytocin. To expand the in vitro results, we further treated oxytocin on adipocytes isolated and induced from mesenchymal stem cells of tibia and femur in mice. After short term treatment of oxytocin, the mRNA expression of FABP4 had the same tendency as in 3T3L1 adipocytes. Taken together, oxytocin may modulate lipid metabolism through decreasing beta oxidation and affecting fatty acid synthesis.