title: Palmitoleic acid (n-7) increases white adipocyte lipolysis and lipase content in a PPARα-dependent manner.
abstract: 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 μM) or palmitic acid (16:0, 200 μM) for 24 h and primary adipocytes from wild-type or PPARα-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 PPARα, was associated with higher rates of PPARα 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 PPARα-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 PPARα-deficient mice. In conclusion, palmitoleic acid increases adipocyte lipolysis and lipases by a mechanism that requires a functional PPARα.
authors.affiliation: Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil;
authors.forename: Andressa
authors.initials: A
authors.lastname: Bolsoni-Lopes
authors.forename: William T
authors.initials: WT
authors.lastname: Festuccia
authors.forename: Talita S M
authors.initials: TS
authors.lastname: Farias
authors.forename: Patricia
authors.initials: P
authors.lastname: Chimin
authors.forename: Francisco L
authors.initials: FL
authors.lastname: Torres-Leal
authors.forename: Priscilla B M
authors.initials: PB
authors.lastname: Derogis
authors.forename: Paula B
authors.initials: PB
authors.lastname: de Andrade
authors.forename: Sayuri
authors.initials: S
authors.lastname: Miyamoto
authors.forename: Fabio B
authors.initials: FB
authors.lastname: Lima
authors.forename: Rui
authors.initials: R
authors.lastname: Curi
authors.forename: Maria Isabel C
authors.initials: MI
authors.lastname: Alonso-Vale
mesh_terms: D041721:3T3-L1 Cells; D052438:Adipocytes, White / Q000187:drug effects* / Q000201:enzymology / Q000378:metabolism; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D015153:Blotting, Western; D001835:Body Weight / Q000187:drug effects; D002469:Cell Separation; D002849:Chromatography, Gas; D005229:Fatty Acids, Monounsaturated / Q000494:pharmacology*; D008049:Lipase / Q000096:biosynthesis / Q000378:metabolism*; D008066:Lipolysis / Q000187:drug effects*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009929:Organ Size / Q000187:drug effects; D047493:PPAR alpha / Q000502:physiology*; D016133:Polymerase Chain Reaction; D002787:Sterol Esterase / Q000096:biosynthesis; D000217:Acyltransferases
chemical_list: D001786:Blood Glucose; D005229:Fatty Acids, Monounsaturated; D008049:Lipase; D047493:PPAR alpha; D002787:Sterol Esterase; C008757:palmitoleic acid; C494445:PNPLA2 protein, mouse; D000217:Acyltransferases
keywords: ATGL; HSL; lipogenesis; triacylglycerol/fatty acid cycle