Distinct Shift in Beta-Cell Glutaredoxin 5 Expression Is Mediated by Hypoxia and Lipotoxicity Both In Vivo and In Vitro.
Identifieur interne : 000272 ( Main/Exploration ); précédent : 000271; suivant : 000273Distinct Shift in Beta-Cell Glutaredoxin 5 Expression Is Mediated by Hypoxia and Lipotoxicity Both In Vivo and In Vitro.
Auteurs : Sebastian Friedrich Petry [Allemagne] ; Lia Mingzhe Sun [Allemagne] ; Anna Knapp [Allemagne] ; Sabrina Reinl [Allemagne] ; Thomas Linn [Allemagne]Source :
- Frontiers in endocrinology [ 1664-2392 ] ; 2018.
Abstract
Histomorphological and functional alterations in pancreatic islet composition directly correlate with hyperglycemia severity. Progressive deterioration of metabolic control in subjects suffering from type 2 diabetes is predominantly caused by impaired beta-cell functionality. The glutaredoxin system is supposed to wield protective properties for beta-cells. Therefore, we sought to identify a correlation between the structural changes observed in diabetic pancreatic islets with altered glutaredoxin 5 expression, in order to determine an underlying mechanism of beta-cell impairment. Islets of db/db mice presenting with uncontrolled diabetes were assessed in terms of morphological structure and insulin, glucagon, and glutaredoxin 5 expression. MIN6 cell function and glutaredoxin 5 expression were analyzed after exposure to oleic acid and hypoxia. Islets of diabese mice were marked by typical remodeling and distinct reduction of, and shifts, in localization of glutaredoxin 5-positive cells. These islets featured decreased glutaredoxin 5 as well as insulin and glucagon content. In beta-cell culture, glutaredoxin 5 protein and mRNA expression were decreased by hypoxia and oleic acid but not by leptin treatment. Our study demonstrates that glutaredoxin 5 expression patterns are distinctively altered in islets of rodents presenting with uncontrolled diabesity. In vitro, reduction of islet-cell glutaredoxin 5 expression was mediated by hypoxia and oleic acid. Thus, glutaredoxin 5-deficiency in islets during diabetes may be caused by lipotoxicity and hypoxia.
DOI: 10.3389/fendo.2018.00084
PubMed: 29593651
PubMed Central: PMC5857561
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Mingzhe" last="Sun">Lia Mingzhe Sun</name><affiliation wicri:level="1"><nlm:affiliation>Clinical Research Unit, Center of Internal Medicine, Justus Liebig University, Giessen, Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Clinical Research Unit, Center of Internal Medicine, Justus Liebig University, Giessen</wicri:regionArea><wicri:noRegion>Giessen</wicri:noRegion><wicri:noRegion>Giessen</wicri:noRegion><wicri:noRegion>Giessen</wicri:noRegion></affiliation></author><author><name sortKey="Knapp, Anna" sort="Knapp, Anna" uniqKey="Knapp A" first="Anna" last="Knapp">Anna Knapp</name><affiliation wicri:level="1"><nlm:affiliation>Clinical Research Unit, Center of Internal Medicine, Justus Liebig University, Giessen, Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Clinical Research Unit, Center of Internal Medicine, Justus Liebig University, 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University, Giessen, Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Clinical Research Unit, Center of Internal Medicine, Justus Liebig University, Giessen</wicri:regionArea><wicri:noRegion>Giessen</wicri:noRegion><wicri:noRegion>Giessen</wicri:noRegion><wicri:noRegion>Giessen</wicri:noRegion></affiliation></author></analytic><series><title level="j">Frontiers in endocrinology</title><idno type="ISSN">1664-2392</idno><imprint><date when="2018" type="published">2018</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Histomorphological and functional alterations in pancreatic islet composition directly correlate with hyperglycemia severity. Progressive deterioration of metabolic control in subjects suffering from type 2 diabetes is predominantly caused by impaired beta-cell functionality. The glutaredoxin system is supposed to wield protective properties for beta-cells. Therefore, we sought to identify a correlation between the structural changes observed in diabetic pancreatic islets with altered glutaredoxin 5 expression, in order to determine an underlying mechanism of beta-cell impairment. Islets of db/db mice presenting with uncontrolled diabetes were assessed in terms of morphological structure and insulin, glucagon, and glutaredoxin 5 expression. MIN6 cell function and glutaredoxin 5 expression were analyzed after exposure to oleic acid and hypoxia. Islets of diabese mice were marked by typical remodeling and distinct reduction of, and shifts, in localization of glutaredoxin 5-positive cells. These islets featured decreased glutaredoxin 5 as well as insulin and glucagon content. In beta-cell culture, glutaredoxin 5 protein and mRNA expression were decreased by hypoxia and oleic acid but not by leptin treatment. Our study demonstrates that glutaredoxin 5 expression patterns are distinctively altered in islets of rodents presenting with uncontrolled diabesity. <i>In vitro</i>, reduction of islet-cell glutaredoxin 5 expression was mediated by hypoxia and oleic acid. Thus, glutaredoxin 5-deficiency in islets during diabetes may be caused by lipotoxicity and hypoxia.</div></front></TEI><pubmed><MedlineCitation Status="PubMed-not-MEDLINE" Owner="NLM"><PMID Version="1">29593651</PMID><DateRevised><Year>2019</Year><Month>11</Month><Day>20</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Print">1664-2392</ISSN><JournalIssue CitedMedium="Print"><Volume>9</Volume><PubDate><Year>2018</Year></PubDate></JournalIssue><Title>Frontiers in endocrinology</Title><ISOAbbreviation>Front Endocrinol (Lausanne)</ISOAbbreviation></Journal><ArticleTitle>Distinct Shift in Beta-Cell Glutaredoxin 5 Expression Is Mediated by Hypoxia and Lipotoxicity Both <i>In Vivo</i> and <i>In Vitro</i>.</ArticleTitle><Pagination><MedlinePgn>84</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.3389/fendo.2018.00084</ELocationID><Abstract><AbstractText>Histomorphological and functional alterations in pancreatic islet composition directly correlate with hyperglycemia severity. Progressive deterioration of metabolic control in subjects suffering from type 2 diabetes is predominantly caused by impaired beta-cell functionality. The glutaredoxin system is supposed to wield protective properties for beta-cells. Therefore, we sought to identify a correlation between the structural changes observed in diabetic pancreatic islets with altered glutaredoxin 5 expression, in order to determine an underlying mechanism of beta-cell impairment. Islets of db/db mice presenting with uncontrolled diabetes were assessed in terms of morphological structure and insulin, glucagon, and glutaredoxin 5 expression. MIN6 cell function and glutaredoxin 5 expression were analyzed after exposure to oleic acid and hypoxia. Islets of diabese mice were marked by typical remodeling and distinct reduction of, and shifts, in localization of glutaredoxin 5-positive cells. These islets featured decreased glutaredoxin 5 as well as insulin and glucagon content. In beta-cell culture, glutaredoxin 5 protein and mRNA expression were decreased by hypoxia and oleic acid but not by leptin treatment. Our study demonstrates that glutaredoxin 5 expression patterns are distinctively altered in islets of rodents presenting with uncontrolled diabesity. <i>In vitro</i>, reduction of islet-cell glutaredoxin 5 expression was mediated by hypoxia and oleic acid. Thus, glutaredoxin 5-deficiency in islets during diabetes may be caused by lipotoxicity and hypoxia.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Petry</LastName><ForeName>Sebastian Friedrich</ForeName><Initials>SF</Initials><AffiliationInfo><Affiliation>Clinical Research Unit, Center of Internal Medicine, Justus Liebig University, Giessen, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sun</LastName><ForeName>Lia Mingzhe</ForeName><Initials>LM</Initials><AffiliationInfo><Affiliation>Clinical Research Unit, Center of Internal Medicine, Justus Liebig University, Giessen, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Knapp</LastName><ForeName>Anna</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Clinical Research Unit, Center of Internal Medicine, Justus Liebig University, Giessen, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Reinl</LastName><ForeName>Sabrina</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Clinical Research Unit, Center of Internal Medicine, Justus Liebig University, Giessen, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Linn</LastName><ForeName>Thomas</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Clinical Research Unit, Center of Internal Medicine, Justus Liebig University, Giessen, Germany.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2018</Year><Month>03</Month><Day>12</Day></ArticleDate></Article><MedlineJournalInfo><Country>Switzerland</Country><MedlineTA>Front Endocrinol (Lausanne)</MedlineTA><NlmUniqueID>101555782</NlmUniqueID><ISSNLinking>1664-2392</ISSNLinking></MedlineJournalInfo><KeywordList Owner="NOTNLM"><Keyword 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Friedrich Petry</name></noRegion><name sortKey="Knapp, Anna" sort="Knapp, Anna" uniqKey="Knapp A" first="Anna" last="Knapp">Anna Knapp</name><name sortKey="Linn, Thomas" sort="Linn, Thomas" uniqKey="Linn T" first="Thomas" last="Linn">Thomas Linn</name><name sortKey="Reinl, Sabrina" sort="Reinl, Sabrina" uniqKey="Reinl S" first="Sabrina" last="Reinl">Sabrina Reinl</name><name sortKey="Sun, Lia Mingzhe" sort="Sun, Lia Mingzhe" uniqKey="Sun L" first="Lia Mingzhe" last="Sun">Lia Mingzhe Sun</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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