| First Author | Bolsoni-Lopes A | Year | 2013 |
| Journal | Am J Physiol Endocrinol Metab | Volume | 305 |
| Issue | 9 | Pages | E1093-102 |
| PubMed ID | 24022867 | Mgi Jnum | J:204511 |
| Mgi Id | MGI:5532754 | Doi | 10.1152/ajpendo.00082.2013 |
| Citation | Bolsoni-Lopes A, et al. (2013) Palmitoleic acid (n-7) increases white adipocyte lipolysis and lipase content in a PPARalpha-dependent manner. Am J Physiol Endocrinol Metab 305(9):E1093-102 |
| abstractText | We investigated whether palmitoleic acid, a fatty acid that enhances whole body glucose disposal and suppresses hepatic steatosis, modulates triacylglycerol (TAG) metabolism in adipocytes. For this, both differentiated 3T3-L1 cells treated with either palmitoleic acid (16:1n7, 200 muM) or palmitic acid (16:0, 200 muM) for 24 h and primary adipocytes from wild-type or PPARalpha-deficient mice treated with 16:1n7 (300 mg.kg(-1).day(-1)) or oleic acid (18:1n9, 300 mg.kg(-1).day(-1)) by gavage for 10 days were evaluated for lipolysis, TAG, and glycerol 3-phosphate synthesis and gene and protein expression profile. Treatment of differentiated 3T3-L1 cells with 16:1n7, but not 16:0, increased basal and isoproterenol-stimulated lipolysis, mRNA levels of adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL) and protein content of ATGL and pSer(660)-HSL. Such increase in lipolysis induced by 16:1n7, which can be prevented by pharmacological inhibition of PPARalpha, was associated with higher rates of PPARalpha binding to DNA. In contrast to lipolysis, both 16:1n7 and 16:0 increased fatty acid incorporation into TAG and glycerol 3-phosphate synthesis from glucose without affecting glyceroneogenesis and glycerokinase expression. Corroborating in vitro findings, treatment of wild-type but not PPARalpha-deficient mice with 16:1n7 increased primary adipocyte basal and stimulated lipolysis and ATGL and HSL mRNA levels. In contrast to lipolysis, however, 16:1n7 treatment increased fatty acid incorporation into TAG and glycerol 3-phosphate synthesis from glucose in both wild-type and PPARalpha-deficient mice. In conclusion, palmitoleic acid increases adipocyte lipolysis and lipases by a mechanism that requires a functional PPARalpha. |
