Palmitoleic acid (n-7) increases white adipocyte lipolysis and lipase content in a PPAR alpha-dependent manner
Autor(a) principal: | |
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Data de Publicação: | 2013 |
Outros Autores: | , , , , , , , , , |
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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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 |
_version_ |
1814268379247149056 |