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
Autor(a) principal: | |
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Data de Publicação: | 2015 |
Outros Autores: | , , , , , , , , , |
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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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 |
|
_version_ |
1808128767040684032 |