Cocoa ameliorates renal injury in Zucker diabetic fatty rats by preventing oxidative stress, apoptosis and inactivation of autophagy.
Identifieur interne : 000235 ( Main/Exploration ); précédent : 000234; suivant : 000236Cocoa ameliorates renal injury in Zucker diabetic fatty rats by preventing oxidative stress, apoptosis and inactivation of autophagy.
Auteurs : David Álvarez-Cilleros [Espagne] ; María Elvira L Pez-Oliva ; María Ngeles Martín ; Sonia RamosSource :
- Food & function [ 2042-650X ] ; 2019.
Descripteurs français
- KwdFr :
- Animaux (MeSH), Apoptose (effets des médicaments et des substances chimiques), Autophagie (effets des médicaments et des substances chimiques), Bécline-1 (génétique), Bécline-1 (métabolisme), Cacaoyer (composition chimique), Catalase (génétique), Catalase (métabolisme), Diabète (génétique), Diabète (métabolisme), Diabète (physiopathologie), Diabète (traitement médicamenteux), Facteur-2 apparenté à NF-E2 (génétique), Facteur-2 apparenté à NF-E2 (métabolisme), Glycémie (métabolisme), Humains (MeSH), Insuline (métabolisme), Mâle (MeSH), Rat Zucker (MeSH), Rats (MeSH), Rein (effets des médicaments et des substances chimiques), Rein (métabolisme), Stress oxydatif (effets des médicaments et des substances chimiques), Superoxide dismutase (génétique), Superoxide dismutase (métabolisme).
- MESH :
- composition chimique : Cacaoyer.
- effets des médicaments et des substances chimiques : Apoptose, Autophagie, Rein, Stress oxydatif.
- génétique : Bécline-1, Catalase, Diabète, Facteur-2 apparenté à NF-E2, Superoxide dismutase.
- métabolisme : Bécline-1, Catalase, Diabète, Facteur-2 apparenté à NF-E2, Glycémie, Insuline, Rein, Superoxide dismutase.
- physiopathologie : Diabète.
- traitement médicamenteux : Diabète.
- Animaux, Humains, Mâle, Rat Zucker, Rats.
English descriptors
- KwdEn :
- Animals (MeSH), Apoptosis (drug effects), Autophagy (drug effects), Beclin-1 (genetics), Beclin-1 (metabolism), Blood Glucose (metabolism), Cacao (chemistry), Catalase (genetics), Catalase (metabolism), Diabetes Mellitus (drug therapy), Diabetes Mellitus (genetics), Diabetes Mellitus (metabolism), Diabetes Mellitus (physiopathology), Humans (MeSH), Insulin (metabolism), Kidney (drug effects), Kidney (metabolism), Male (MeSH), NF-E2-Related Factor 2 (genetics), NF-E2-Related Factor 2 (metabolism), Oxidative Stress (drug effects), Rats (MeSH), Rats, Zucker (MeSH), Superoxide Dismutase (genetics), Superoxide Dismutase (metabolism).
- MESH :
- chemical , genetics : Beclin-1, Catalase, NF-E2-Related Factor 2, Superoxide Dismutase.
- chemistry : Cacao.
- drug effects : Apoptosis, Autophagy, Kidney, Oxidative Stress.
- drug therapy : Diabetes Mellitus.
- genetics : Diabetes Mellitus.
- chemical , metabolism : Beclin-1, Blood Glucose, Catalase, Diabetes Mellitus, Insulin, Kidney, NF-E2-Related Factor 2, Superoxide Dismutase.
- physiopathology : Diabetes Mellitus.
- Animals, Humans, Male, Rats, Rats, Zucker.
Abstract
Redox balance, autophagy and apoptosis are main processes involved in the development of diabetic nephropathy. Epidemiological and animal studies suggest that cocoa might reduce the risk of diabetic complications. However, the molecular mechanisms responsible for these potential preventive activities and whether cocoa exerts beneficial effects on dysregulated signalling pathways involved in cellular antioxidant defence, autophagy and apoptosis in the diabetic kidney remain largely unknown. Therefore, this work investigated the effect of a cocoa-rich diet on the mentioned processes in the renal cortex of Zucker Diabetic Fatty (ZDF) rats. Male ZDF rats were fed either a control or cocoa-rich diet (10%), and Zucker lean animals received the control diet (10-20 weeks-of-life). ZDF rats fed with cocoa decreased body weight and glucose and insulin levels, and improved renal function. Cocoa intake further prevented the enhanced renal cortical oxidative stress in diabetic rats by regulating the antioxidant defence system and close-related proteins to cytoprotection and cell response; thus, cocoa diminished oxidative markers (reactive oxygen species and carbonyl groups) and NADPH-oxidase-4 levels, and restored key enzymatic antioxidant activities (superoxide dismutase and catalase), nuclear-erythroid-2-related factor-2, and ERK-MAPK levels, as well as sirtuin-1/5'-AMP-activated-protein kinase signalling. Moreover, in ZDF rats cocoa-rich diet contributed to alleviation of the renal cortical injury through autophagy activation (p62 upregulation, and downregulation of beclin-1 and LC3), and inhibition of apoptosis (Bcl-xL stimulation and suppression of Bax and caspases-9 and -3). These findings provide the first in vivo evidence on the molecular mechanisms of cocoa to circumvent renal cortical damage that involve improvement of antioxidant competences, stimulation of autophagy and suppression of apoptosis in ZDF rats.
DOI: 10.1039/c9fo01806a
PubMed: 31773121
Affiliations:
Links toward previous steps (curation, corpus...)
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(métabolisme)</term><term>Stress oxydatif (effets des médicaments et des substances chimiques)</term><term>Superoxide dismutase (génétique)</term><term>Superoxide dismutase (métabolisme)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Beclin-1</term><term>Catalase</term><term>NF-E2-Related Factor 2</term><term>Superoxide Dismutase</term></keywords><keywords scheme="MESH" qualifier="chemistry" xml:lang="en"><term>Cacao</term></keywords><keywords scheme="MESH" qualifier="composition chimique" xml:lang="fr"><term>Cacaoyer</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Apoptosis</term><term>Autophagy</term><term>Kidney</term><term>Oxidative Stress</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Diabetes Mellitus</term></keywords><keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Apoptose</term><term>Autophagie</term><term>Rein</term><term>Stress oxydatif</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Diabetes Mellitus</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Bécline-1</term><term>Catalase</term><term>Diabète</term><term>Facteur-2 apparenté à NF-E2</term><term>Superoxide dismutase</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Beclin-1</term><term>Blood Glucose</term><term>Catalase</term><term>Diabetes Mellitus</term><term>Insulin</term><term>Kidney</term><term>NF-E2-Related Factor 2</term><term>Superoxide Dismutase</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Bécline-1</term><term>Catalase</term><term>Diabète</term><term>Facteur-2 apparenté à NF-E2</term><term>Glycémie</term><term>Insuline</term><term>Rein</term><term>Superoxide dismutase</term></keywords><keywords scheme="MESH" qualifier="physiopathologie" xml:lang="fr"><term>Diabète</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Diabetes Mellitus</term></keywords><keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Diabète</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Humans</term><term>Male</term><term>Rats</term><term>Rats, Zucker</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Humains</term><term>Mâle</term><term>Rat Zucker</term><term>Rats</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Redox balance, autophagy and apoptosis are main processes involved in the development of diabetic nephropathy. Epidemiological and animal studies suggest that cocoa might reduce the risk of diabetic complications. However, the molecular mechanisms responsible for these potential preventive activities and whether cocoa exerts beneficial effects on dysregulated signalling pathways involved in cellular antioxidant defence, autophagy and apoptosis in the diabetic kidney remain largely unknown. Therefore, this work investigated the effect of a cocoa-rich diet on the mentioned processes in the renal cortex of Zucker Diabetic Fatty (ZDF) rats. Male ZDF rats were fed either a control or cocoa-rich diet (10%), and Zucker lean animals received the control diet (10-20 weeks-of-life). ZDF rats fed with cocoa decreased body weight and glucose and insulin levels, and improved renal function. Cocoa intake further prevented the enhanced renal cortical oxidative stress in diabetic rats by regulating the antioxidant defence system and close-related proteins to cytoprotection and cell response; thus, cocoa diminished oxidative markers (reactive oxygen species and carbonyl groups) and NADPH-oxidase-4 levels, and restored key enzymatic antioxidant activities (superoxide dismutase and catalase), nuclear-erythroid-2-related factor-2, and ERK-MAPK levels, as well as sirtuin-1/5'-AMP-activated-protein kinase signalling. Moreover, in ZDF rats cocoa-rich diet contributed to alleviation of the renal cortical injury through autophagy activation (p62 upregulation, and downregulation of beclin-1 and LC3), and inhibition of apoptosis (Bcl-xL stimulation and suppression of Bax and caspases-9 and -3). These findings provide the first in vivo evidence on the molecular mechanisms of cocoa to circumvent renal cortical damage that involve improvement of antioxidant competences, stimulation of autophagy and suppression of apoptosis in ZDF rats.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">31773121</PMID><DateCompleted><Year>2020</Year><Month>04</Month><Day>16</Day></DateCompleted><DateRevised><Year>2020</Year><Month>04</Month><Day>16</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">2042-650X</ISSN><JournalIssue CitedMedium="Internet"><Volume>10</Volume><Issue>12</Issue><PubDate><Year>2019</Year><Month>Dec</Month><Day>11</Day></PubDate></JournalIssue><Title>Food & function</Title><ISOAbbreviation>Food Funct</ISOAbbreviation></Journal><ArticleTitle>Cocoa ameliorates renal injury in Zucker diabetic fatty rats by preventing oxidative stress, apoptosis and inactivation of autophagy.</ArticleTitle><Pagination><MedlinePgn>7926-7939</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1039/c9fo01806a</ELocationID><Abstract><AbstractText>Redox balance, autophagy and apoptosis are main processes involved in the development of diabetic nephropathy. Epidemiological and animal studies suggest that cocoa might reduce the risk of diabetic complications. However, the molecular mechanisms responsible for these potential preventive activities and whether cocoa exerts beneficial effects on dysregulated signalling pathways involved in cellular antioxidant defence, autophagy and apoptosis in the diabetic kidney remain largely unknown. Therefore, this work investigated the effect of a cocoa-rich diet on the mentioned processes in the renal cortex of Zucker Diabetic Fatty (ZDF) rats. Male ZDF rats were fed either a control or cocoa-rich diet (10%), and Zucker lean animals received the control diet (10-20 weeks-of-life). ZDF rats fed with cocoa decreased body weight and glucose and insulin levels, and improved renal function. Cocoa intake further prevented the enhanced renal cortical oxidative stress in diabetic rats by regulating the antioxidant defence system and close-related proteins to cytoprotection and cell response; thus, cocoa diminished oxidative markers (reactive oxygen species and carbonyl groups) and NADPH-oxidase-4 levels, and restored key enzymatic antioxidant activities (superoxide dismutase and catalase), nuclear-erythroid-2-related factor-2, and ERK-MAPK levels, as well as sirtuin-1/5'-AMP-activated-protein kinase signalling. Moreover, in ZDF rats cocoa-rich diet contributed to alleviation of the renal cortical injury through autophagy activation (p62 upregulation, and downregulation of beclin-1 and LC3), and inhibition of apoptosis (Bcl-xL stimulation and suppression of Bax and caspases-9 and -3). These findings provide the first in vivo evidence on the molecular mechanisms of cocoa to circumvent renal cortical damage that involve improvement of antioxidant competences, stimulation of autophagy and suppression of apoptosis in ZDF rats.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Álvarez-Cilleros</LastName><ForeName>David</ForeName><Initials>D</Initials><Suffix></Suffix><AffiliationInfo><Affiliation>Department of Metabolism and Nutrition, Institute of Food Science and Technology and Nutrition (ICTAN), Consejo Superior de Investigaciones Científicas (CSIC), José Antonio Novais 10, Ciudad Universitaria, 28040 Madrid, Spain. s.ramos@ictan.csic.es.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>López-Oliva</LastName><ForeName>María Elvira</ForeName><Initials>ME</Initials><Suffix></Suffix></Author><Author ValidYN="Y"><LastName>Martín</LastName><ForeName>María Ángeles</ForeName><Initials>MÁ</Initials><Suffix></Suffix></Author><Author ValidYN="Y"><LastName>Ramos</LastName><ForeName>Sonia</ForeName><Initials>S</Initials><Suffix></Suffix></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Food Funct</MedlineTA><NlmUniqueID>101549033</NlmUniqueID><ISSNLinking>2042-6496</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000071186">Beclin-1</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001786">Blood Glucose</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007328">Insulin</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051267">NF-E2-Related Factor 2</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C495636">Nfe2l2 protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.11.1.6</RegistryNumber><NameOfSubstance UI="D002374">Catalase</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.15.1.1</RegistryNumber><NameOfSubstance UI="D013482">Superoxide Dismutase</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017209" MajorTopicYN="N">Apoptosis</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001343" MajorTopicYN="N">Autophagy</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000071186" MajorTopicYN="N">Beclin-1</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001786" MajorTopicYN="N">Blood Glucose</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002099" MajorTopicYN="N">Cacao</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="Y">chemistry</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002374" MajorTopicYN="N">Catalase</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003920" MajorTopicYN="N">Diabetes Mellitus</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007328" MajorTopicYN="N">Insulin</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007668" MajorTopicYN="N">Kidney</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051267" MajorTopicYN="N">NF-E2-Related Factor 2</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" 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Ramos</name></noCountry><country name="Espagne"><region name="Communauté de Madrid"><name sortKey="Alvarez Cilleros, David" sort="Alvarez Cilleros, David" uniqKey="Alvarez Cilleros D" first="David" last="Álvarez-Cilleros">David Álvarez-Cilleros</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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