Decaffeinated green tea extract rich in epigallocatechin-3-gallate prevents fatty liver disease by increased activities of mitochondrial respiratory chain complexes in diet-induced obesity mice

Detalhes bibliográficos
Autor(a) principal: Santamarina, Aline B.
Data de Publicação: 2015
Outros Autores: Carvalho-Silva, Milena, Gomes, Lara M., Okuda, Marcos H., Santana, Aline A., Streck, Emilio L., Seelaender, Marilia, Oller do Nascimento, Claudia M., Ribeiro, Eliane B., Lira, Fabio S. [UNESP], Oyama, Lila Missae
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Institucional da UNESP
Texto Completo: http://dx.doi.org/10.1016/j.jnutbio.2015.07.002
http://hdl.handle.net/11449/160981
Resumo: Nonalcoholic fatty liver disease has been considered the hepatic manifestation of obesity. It is unclear whether supplementation with green tea extract rich in epigallocatechin-3-gallate (EGCG) influences the activity of mitochondrial respiratory chain complexes and insulin resistance in the liver. EGCG regulated hepatic mitochondrial respiratory chain complexes and was capable of improving lipid metabolism, attenuating insulin resistance in obese mice. Mice were divided into four groups: control diet+water (CW) or EGCG (CE) and hyperlipidic diet+water (HFW) or EGCG (HFE). All animals received water and diets ad libitum for 16 weeks. Placebo groups received water (0.1 ml/day) and EGCG groups (0.1 ml EGCG and 50 mg/kg/day) by gavage. Cytokines concentrations were obtained by EUSA, protein expression through Western blotting and mitochondrial complex enzymatic activity by calorimetric assay of substrate degradation. HFW increased body weight gain, adiposity index, retroperitoneal and mesenteric adipose tissue relative weight, serum glucose, insulin and Homeostasis Model Assessment of Basal Insulin Resistance (HOMA-IR); glucose intolerance was observed in oral glucose tolerance test (OGTT) as well as ectopic fat liver deposition. HFE group decreased body weight gain, retroperitoneal and mesenteric adipose tissue relative weight, HOMA-IR, insulin levels and liver fat accumulation; increased complexes II-III and IV and malate dehydrogenase activities and improvement in glucose uptake in OGTT and insulin sensitivity by increased protein expression of total AKT, IR alpha and IRS1. We did not find alterations in inflammatory parameters analyzed. EGCG was able to prevent obesity stimulating the mitochondrial complex chain, increasing energy expenditure, particularly from the oxidation of lipid substrates, thereby contributing to the prevention of hepatic steatosis and improved insulin sensitivity. (C) 2015 Elsevier Inc. All rights reserved.
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spelling Decaffeinated green tea extract rich in epigallocatechin-3-gallate prevents fatty liver disease by increased activities of mitochondrial respiratory chain complexes in diet-induced obesity miceEGCGNAFLDObesityMiceRespiratory chainInsulin resistanceNonalcoholic fatty liver disease has been considered the hepatic manifestation of obesity. It is unclear whether supplementation with green tea extract rich in epigallocatechin-3-gallate (EGCG) influences the activity of mitochondrial respiratory chain complexes and insulin resistance in the liver. EGCG regulated hepatic mitochondrial respiratory chain complexes and was capable of improving lipid metabolism, attenuating insulin resistance in obese mice. Mice were divided into four groups: control diet+water (CW) or EGCG (CE) and hyperlipidic diet+water (HFW) or EGCG (HFE). All animals received water and diets ad libitum for 16 weeks. Placebo groups received water (0.1 ml/day) and EGCG groups (0.1 ml EGCG and 50 mg/kg/day) by gavage. Cytokines concentrations were obtained by EUSA, protein expression through Western blotting and mitochondrial complex enzymatic activity by calorimetric assay of substrate degradation. HFW increased body weight gain, adiposity index, retroperitoneal and mesenteric adipose tissue relative weight, serum glucose, insulin and Homeostasis Model Assessment of Basal Insulin Resistance (HOMA-IR); glucose intolerance was observed in oral glucose tolerance test (OGTT) as well as ectopic fat liver deposition. HFE group decreased body weight gain, retroperitoneal and mesenteric adipose tissue relative weight, HOMA-IR, insulin levels and liver fat accumulation; increased complexes II-III and IV and malate dehydrogenase activities and improvement in glucose uptake in OGTT and insulin sensitivity by increased protein expression of total AKT, IR alpha and IRS1. We did not find alterations in inflammatory parameters analyzed. EGCG was able to prevent obesity stimulating the mitochondrial complex chain, increasing energy expenditure, particularly from the oxidation of lipid substrates, thereby contributing to the prevention of hepatic steatosis and improved insulin sensitivity. (C) 2015 Elsevier Inc. All rights reserved.Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Univ Fed Sao Paulo, Dept Fisiol, BR-04021001 Sao Paulo, SP, BrazilUniv Extremo Sul Catarinense, Programa Posgrad Ciencia Saude, BR-88806000 Criciuma, SC, BrazilUniv Sao Paulo, Inst Biomed Sci, Canc Metab Res Grp, BR-05508000 Sao Paulo, SP, BrazilUniv Estadual Paulista, Dept Phys Educ, Exercise & Immunometab Res Grp, BR-19060900 Presidente Prudente, SP, BrazilUniv Estadual Paulista, Dept Phys Educ, Exercise & Immunometab Res Grp, BR-19060900 Presidente Prudente, SP, BrazilFAPESP: 2014/19508-7Elsevier B.V.Universidade Federal de São Paulo (UNIFESP)Univ Extremo Sul CatarinenseUniversidade de São Paulo (USP)Universidade Estadual Paulista (Unesp)Santamarina, Aline B.Carvalho-Silva, MilenaGomes, Lara M.Okuda, Marcos H.Santana, Aline A.Streck, Emilio L.Seelaender, MariliaOller do Nascimento, Claudia M.Ribeiro, Eliane B.Lira, Fabio S. [UNESP]Oyama, Lila Missae2018-11-26T16:17:29Z2018-11-26T16:17:29Z2015-11-01info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/article1348-1356application/pdfhttp://dx.doi.org/10.1016/j.jnutbio.2015.07.002Journal Of Nutritional Biochemistry. New York: Elsevier Science Inc, v. 26, n. 11, p. 1348-1356, 2015.0955-2863http://hdl.handle.net/11449/16098110.1016/j.jnutbio.2015.07.002WOS:000364979600025WOS000364979600025.pdfWeb of Sciencereponame:Repositório Institucional da UNESPinstname:Universidade Estadual Paulista (UNESP)instacron:UNESPengJournal Of Nutritional Biochemistry1,678info:eu-repo/semantics/openAccess2024-06-18T17:42:46Zoai:repositorio.unesp.br:11449/160981Repositório InstitucionalPUBhttp://repositorio.unesp.br/oai/requestopendoar:29462024-08-05T17:10:52.489573Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)false
dc.title.none.fl_str_mv Decaffeinated green tea extract rich in epigallocatechin-3-gallate prevents fatty liver disease by increased activities of mitochondrial respiratory chain complexes in diet-induced obesity mice
title Decaffeinated green tea extract rich in epigallocatechin-3-gallate prevents fatty liver disease by increased activities of mitochondrial respiratory chain complexes in diet-induced obesity mice
spellingShingle Decaffeinated green tea extract rich in epigallocatechin-3-gallate prevents fatty liver disease by increased activities of mitochondrial respiratory chain complexes in diet-induced obesity mice
Santamarina, Aline B.
EGCG
NAFLD
Obesity
Mice
Respiratory chain
Insulin resistance
title_short Decaffeinated green tea extract rich in epigallocatechin-3-gallate prevents fatty liver disease by increased activities of mitochondrial respiratory chain complexes in diet-induced obesity mice
title_full Decaffeinated green tea extract rich in epigallocatechin-3-gallate prevents fatty liver disease by increased activities of mitochondrial respiratory chain complexes in diet-induced obesity mice
title_fullStr Decaffeinated green tea extract rich in epigallocatechin-3-gallate prevents fatty liver disease by increased activities of mitochondrial respiratory chain complexes in diet-induced obesity mice
title_full_unstemmed Decaffeinated green tea extract rich in epigallocatechin-3-gallate prevents fatty liver disease by increased activities of mitochondrial respiratory chain complexes in diet-induced obesity mice
title_sort Decaffeinated green tea extract rich in epigallocatechin-3-gallate prevents fatty liver disease by increased activities of mitochondrial respiratory chain complexes in diet-induced obesity mice
author Santamarina, Aline B.
author_facet Santamarina, Aline B.
Carvalho-Silva, Milena
Gomes, Lara M.
Okuda, Marcos H.
Santana, Aline A.
Streck, Emilio L.
Seelaender, Marilia
Oller do Nascimento, Claudia M.
Ribeiro, Eliane B.
Lira, Fabio S. [UNESP]
Oyama, Lila Missae
author_role author
author2 Carvalho-Silva, Milena
Gomes, Lara M.
Okuda, Marcos H.
Santana, Aline A.
Streck, Emilio L.
Seelaender, Marilia
Oller do Nascimento, Claudia M.
Ribeiro, Eliane B.
Lira, Fabio S. [UNESP]
Oyama, Lila Missae
author2_role author
author
author
author
author
author
author
author
author
author
dc.contributor.none.fl_str_mv Universidade Federal de São Paulo (UNIFESP)
Univ Extremo Sul Catarinense
Universidade de São Paulo (USP)
Universidade Estadual Paulista (Unesp)
dc.contributor.author.fl_str_mv Santamarina, Aline B.
Carvalho-Silva, Milena
Gomes, Lara M.
Okuda, Marcos H.
Santana, Aline A.
Streck, Emilio L.
Seelaender, Marilia
Oller do Nascimento, Claudia M.
Ribeiro, Eliane B.
Lira, Fabio S. [UNESP]
Oyama, Lila Missae
dc.subject.por.fl_str_mv EGCG
NAFLD
Obesity
Mice
Respiratory chain
Insulin resistance
topic EGCG
NAFLD
Obesity
Mice
Respiratory chain
Insulin resistance
description Nonalcoholic fatty liver disease has been considered the hepatic manifestation of obesity. It is unclear whether supplementation with green tea extract rich in epigallocatechin-3-gallate (EGCG) influences the activity of mitochondrial respiratory chain complexes and insulin resistance in the liver. EGCG regulated hepatic mitochondrial respiratory chain complexes and was capable of improving lipid metabolism, attenuating insulin resistance in obese mice. Mice were divided into four groups: control diet+water (CW) or EGCG (CE) and hyperlipidic diet+water (HFW) or EGCG (HFE). All animals received water and diets ad libitum for 16 weeks. Placebo groups received water (0.1 ml/day) and EGCG groups (0.1 ml EGCG and 50 mg/kg/day) by gavage. Cytokines concentrations were obtained by EUSA, protein expression through Western blotting and mitochondrial complex enzymatic activity by calorimetric assay of substrate degradation. HFW increased body weight gain, adiposity index, retroperitoneal and mesenteric adipose tissue relative weight, serum glucose, insulin and Homeostasis Model Assessment of Basal Insulin Resistance (HOMA-IR); glucose intolerance was observed in oral glucose tolerance test (OGTT) as well as ectopic fat liver deposition. HFE group decreased body weight gain, retroperitoneal and mesenteric adipose tissue relative weight, HOMA-IR, insulin levels and liver fat accumulation; increased complexes II-III and IV and malate dehydrogenase activities and improvement in glucose uptake in OGTT and insulin sensitivity by increased protein expression of total AKT, IR alpha and IRS1. We did not find alterations in inflammatory parameters analyzed. EGCG was able to prevent obesity stimulating the mitochondrial complex chain, increasing energy expenditure, particularly from the oxidation of lipid substrates, thereby contributing to the prevention of hepatic steatosis and improved insulin sensitivity. (C) 2015 Elsevier Inc. All rights reserved.
publishDate 2015
dc.date.none.fl_str_mv 2015-11-01
2018-11-26T16:17:29Z
2018-11-26T16:17:29Z
dc.type.status.fl_str_mv info:eu-repo/semantics/publishedVersion
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
format article
status_str publishedVersion
dc.identifier.uri.fl_str_mv http://dx.doi.org/10.1016/j.jnutbio.2015.07.002
Journal Of Nutritional Biochemistry. New York: Elsevier Science Inc, v. 26, n. 11, p. 1348-1356, 2015.
0955-2863
http://hdl.handle.net/11449/160981
10.1016/j.jnutbio.2015.07.002
WOS:000364979600025
WOS000364979600025.pdf
url http://dx.doi.org/10.1016/j.jnutbio.2015.07.002
http://hdl.handle.net/11449/160981
identifier_str_mv Journal Of Nutritional Biochemistry. New York: Elsevier Science Inc, v. 26, n. 11, p. 1348-1356, 2015.
0955-2863
10.1016/j.jnutbio.2015.07.002
WOS:000364979600025
WOS000364979600025.pdf
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv Journal Of Nutritional Biochemistry
1,678
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv 1348-1356
application/pdf
dc.publisher.none.fl_str_mv Elsevier B.V.
publisher.none.fl_str_mv Elsevier B.V.
dc.source.none.fl_str_mv Web of Science
reponame:Repositório Institucional da UNESP
instname:Universidade Estadual Paulista (UNESP)
instacron:UNESP
instname_str Universidade Estadual Paulista (UNESP)
instacron_str UNESP
institution UNESP
reponame_str Repositório Institucional da UNESP
collection Repositório Institucional da UNESP
repository.name.fl_str_mv Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)
repository.mail.fl_str_mv
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