Palmitoleic acid (n-7) increases white adipocyte lipolysis and lipase content in a PPAR alpha-dependent manner

Detalhes bibliográficos
Autor(a) principal: Bolsoni-Lopes, Andressa
Data de Publicação: 2013
Outros Autores: Festuccia, William T., Farias, Talita S. M., Chimin, Patricia, Torres-Leal, Francisco L., Derogis, Priscilla B. M., Andrade, Paula B. de, Miyamoto, Sayuri, Lima, Fabio B., Curi, Rui, Alonso-Vale, Maria Isabel C. [UNIFESP]
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Institucional da UNIFESP
Texto Completo: http://dx.doi.org/10.1152/ajpendo.00082.2013
http://repositorio.unifesp.br/handle/11600/36907
Resumo: 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 mu M) or palmitic acid (16: 0, 200 mu M) for 24 h and primary adipocytes from wild-type or PPAR alpha-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 PPAR alpha, was associated with higher rates of PPAR alpha 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 PPAR alpha-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 PPAR alpha-deficient mice. in conclusion, palmitoleic acid increases adipocyte lipolysis and lipases by a mechanism that requires a functional PPAR alpha.
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spelling Palmitoleic acid (n-7) increases white adipocyte lipolysis and lipase content in a PPAR alpha-dependent mannerATGLHSLlipogenesistriacylglycerol/fatty acid cycleWe 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 mu M) or palmitic acid (16: 0, 200 mu M) for 24 h and primary adipocytes from wild-type or PPAR alpha-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 PPAR alpha, was associated with higher rates of PPAR alpha 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 PPAR alpha-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 PPAR alpha-deficient mice. in conclusion, palmitoleic acid increases adipocyte lipolysis and lipases by a mechanism that requires a functional PPAR alpha.Univ São Paulo, Inst Biomed Sci, Dept Physiol & Biophys, São Paulo, BrazilUniv São Paulo, Inst Chem, Dept Biochem, São Paulo, BrazilUniversidade Federal de São Paulo, Inst Environm Sci Chem & Pharmaceut, Dept Biol Sci, BR-09913030 Diadema, BrazilUniversidade Federal de São Paulo, Inst Environm Sci Chem & Pharmaceut, Dept Biol Sci, BR-09913030 Diadema, BrazilWeb of ScienceFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)FAPESP: 2011/51627-8FAPESP: 2009/15354-7FAPESP: 2010/10909-8FAPESP: 2009/53964-1Amer Physiological SocUniversidade de São Paulo (USP)Universidade Federal de São Paulo (UNIFESP)Bolsoni-Lopes, AndressaFestuccia, William T.Farias, Talita S. M.Chimin, PatriciaTorres-Leal, Francisco L.Derogis, Priscilla B. M.Andrade, Paula B. deMiyamoto, SayuriLima, Fabio B.Curi, RuiAlonso-Vale, Maria Isabel C. [UNIFESP]2016-01-24T14:34:38Z2016-01-24T14:34:38Z2013-11-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionE1093-E1102http://dx.doi.org/10.1152/ajpendo.00082.2013American Journal of Physiology-endocrinology and Metabolism. Bethesda: Amer Physiological Soc, v. 305, n. 9, p. E1093-E1102, 2013.10.1152/ajpendo.00082.20130193-1849http://repositorio.unifesp.br/handle/11600/36907WOS:000326578600005engAmerican Journal of Physiology-endocrinology and Metabolisminfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UNIFESPinstname:Universidade Federal de São Paulo (UNIFESP)instacron:UNIFESP2016-01-24T12:34:38Zoai:repositorio.unifesp.br/:11600/36907Repositório InstitucionalPUBhttp://www.repositorio.unifesp.br/oai/requestbiblioteca.csp@unifesp.bropendoar:34652016-01-24T12:34:38Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)false
dc.title.none.fl_str_mv Palmitoleic acid (n-7) increases white adipocyte lipolysis and lipase content in a PPAR alpha-dependent manner
title Palmitoleic acid (n-7) increases white adipocyte lipolysis and lipase content in a PPAR alpha-dependent manner
spellingShingle Palmitoleic acid (n-7) increases white adipocyte lipolysis and lipase content in a PPAR alpha-dependent manner
Bolsoni-Lopes, Andressa
ATGL
HSL
lipogenesis
triacylglycerol/fatty acid cycle
title_short Palmitoleic acid (n-7) increases white adipocyte lipolysis and lipase content in a PPAR alpha-dependent manner
title_full Palmitoleic acid (n-7) increases white adipocyte lipolysis and lipase content in a PPAR alpha-dependent manner
title_fullStr Palmitoleic acid (n-7) increases white adipocyte lipolysis and lipase content in a PPAR alpha-dependent manner
title_full_unstemmed Palmitoleic acid (n-7) increases white adipocyte lipolysis and lipase content in a PPAR alpha-dependent manner
title_sort Palmitoleic acid (n-7) increases white adipocyte lipolysis and lipase content in a PPAR alpha-dependent manner
author Bolsoni-Lopes, Andressa
author_facet Bolsoni-Lopes, Andressa
Festuccia, William T.
Farias, Talita S. M.
Chimin, Patricia
Torres-Leal, Francisco L.
Derogis, Priscilla B. M.
Andrade, Paula B. de
Miyamoto, Sayuri
Lima, Fabio B.
Curi, Rui
Alonso-Vale, Maria Isabel C. [UNIFESP]
author_role author
author2 Festuccia, William T.
Farias, Talita S. M.
Chimin, Patricia
Torres-Leal, Francisco L.
Derogis, Priscilla B. M.
Andrade, Paula B. de
Miyamoto, Sayuri
Lima, Fabio B.
Curi, Rui
Alonso-Vale, Maria Isabel C. [UNIFESP]
author2_role author
author
author
author
author
author
author
author
author
author
dc.contributor.none.fl_str_mv Universidade de São Paulo (USP)
Universidade Federal de São Paulo (UNIFESP)
dc.contributor.author.fl_str_mv Bolsoni-Lopes, Andressa
Festuccia, William T.
Farias, Talita S. M.
Chimin, Patricia
Torres-Leal, Francisco L.
Derogis, Priscilla B. M.
Andrade, Paula B. de
Miyamoto, Sayuri
Lima, Fabio B.
Curi, Rui
Alonso-Vale, Maria Isabel C. [UNIFESP]
dc.subject.por.fl_str_mv ATGL
HSL
lipogenesis
triacylglycerol/fatty acid cycle
topic ATGL
HSL
lipogenesis
triacylglycerol/fatty acid cycle
description 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 mu M) or palmitic acid (16: 0, 200 mu M) for 24 h and primary adipocytes from wild-type or PPAR alpha-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 PPAR alpha, was associated with higher rates of PPAR alpha 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 PPAR alpha-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 PPAR alpha-deficient mice. in conclusion, palmitoleic acid increases adipocyte lipolysis and lipases by a mechanism that requires a functional PPAR alpha.
publishDate 2013
dc.date.none.fl_str_mv 2013-11-01
2016-01-24T14:34:38Z
2016-01-24T14:34:38Z
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
dc.type.status.fl_str_mv info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.uri.fl_str_mv http://dx.doi.org/10.1152/ajpendo.00082.2013
American Journal of Physiology-endocrinology and Metabolism. Bethesda: Amer Physiological Soc, v. 305, n. 9, p. E1093-E1102, 2013.
10.1152/ajpendo.00082.2013
0193-1849
http://repositorio.unifesp.br/handle/11600/36907
WOS:000326578600005
url http://dx.doi.org/10.1152/ajpendo.00082.2013
http://repositorio.unifesp.br/handle/11600/36907
identifier_str_mv American Journal of Physiology-endocrinology and Metabolism. Bethesda: Amer Physiological Soc, v. 305, n. 9, p. E1093-E1102, 2013.
10.1152/ajpendo.00082.2013
0193-1849
WOS:000326578600005
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv American Journal of Physiology-endocrinology and Metabolism
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv E1093-E1102
dc.publisher.none.fl_str_mv Amer Physiological Soc
publisher.none.fl_str_mv Amer Physiological Soc
dc.source.none.fl_str_mv reponame:Repositório Institucional da UNIFESP
instname:Universidade Federal de São Paulo (UNIFESP)
instacron:UNIFESP
instname_str Universidade Federal de São Paulo (UNIFESP)
instacron_str UNIFESP
institution UNIFESP
reponame_str Repositório Institucional da UNIFESP
collection Repositório Institucional da UNIFESP
repository.name.fl_str_mv Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)
repository.mail.fl_str_mv biblioteca.csp@unifesp.br
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