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Conference Paper: Amelioration of hyperglycemia-induced mitochondrial ROS generation of single pancreatic islet β-cells of obese/diabetic mice by chronic N-Acetyl-L-Cysteine

TitleAmelioration of hyperglycemia-induced mitochondrial ROS generation of single pancreatic islet β-cells of obese/diabetic mice by chronic N-Acetyl-L-Cysteine
Authors
KeywordsCardiovascular disease
Issue Date2009
PublisherHong Kong College of Cardiology. The Journal's web site is located at http://www.hkcchk.com/journals.php#3
Citation
The 13th Annual Scientific Meeting Institute of Cardiovascular Science and Medicine (ICSM), Hong Kong, 12 December 2009. In Journal of the Hong Kong College of Cardiology, 2009, v. 17 n. 2, p. 59, abstract P12 How to Cite?
AbstractBACKGROUND: Mitochondria are the principal source of reactive oxygen species (ROS) in pancreatic islets β-cells and impairment of mitochondrial functions is intrinsically related with diabetes mellitus. Hyperglycemiainduced ROS production by mitochondria is an important aspect in β-cell glucose toxicity. However, most previous studies were performed in either normal islets/single β-cells or insulinoma cells which were bathed in high glucose medium which could not mimic the pathophysiological conditions. OBJECTIVES: To compare and measure hyperglycemia-induced mitochondria ROS generation of primary pancreatic islet β-cells of obese/diabetic (+db/+db) and lean/control (+db/+m) mice, and the effects (acute and chronic) of N-acetyl-L-cysteine (NAC) on ROS generation. METHODS: Collagenase-dissociated single pancreatic islet β-cells of C57BL/KsJ obese/diabetic (+db/+db) mice which exhibit phenotypes of the human T2DM were harvested, and the effects (acute, 10 min; chronic, 24 h) of NAC (20 mM) on high glucose-induced mitochondrial ROS generation were evaluated. Mitochondrial ROS levels were estimated by MitoTracker Red (reduced form) (a selective fluorescence probe for mitochondrial ROS measurement) using con-focal microscope. RESULTS: A trend of, but a non-significant, higher resting/basal ROS level was observed in single pancreatic β-cells of +db/+db mice compared to +db/+m mice. High glucose (15 mM) application gradually caused an increase in ROS levels in single pancreatic β-cells of +db/+db mice whereas no apparent change was observed in +db/+m mice. Chronic (24 h), but not acute (10 min), treatments with NAC (20 mM) ameliorated high-glucose induced ROS generation in single pancreatic β-cells of +db/+db mice. CONCLUSIONS: Hyperglycemia elicited mitochondrial ROS generation only in single pancreatic β-cells of +db/+db mice. Chronic NAC (a well known anti-oxidant) pre-treatment eradicated high glucose-induced ROS generation. Current study is underway to elucidate the underlying mechanism(s) involved in the differential effects of high glucose on ROS generation as well as the identification of the particular mitochondrial ROS generating system.
DescriptionThis journal issue contain abstracts of the 13th Annual Scientific Meeting of the Institute of Cardiovascular Science and Medicine 2009
Abstracts for Posters: P12
Persistent Identifierhttp://hdl.handle.net/10722/106880
ISSN
2015 SCImago Journal Rankings: 0.102

 

DC FieldValueLanguage
dc.contributor.authorPoon, CCWen_HK
dc.contributor.authorAu, ALSen_HK
dc.contributor.authorZhang, TQen_HK
dc.contributor.authorKong, SKen_HK
dc.contributor.authorHo, AHPen_HK
dc.contributor.authorLeung, GPHen_HK
dc.contributor.authorKwan, YWen_HK
dc.date.accessioned2010-09-25T23:34:19Z-
dc.date.available2010-09-25T23:34:19Z-
dc.date.issued2009en_HK
dc.identifier.citationThe 13th Annual Scientific Meeting Institute of Cardiovascular Science and Medicine (ICSM), Hong Kong, 12 December 2009. In Journal of the Hong Kong College of Cardiology, 2009, v. 17 n. 2, p. 59, abstract P12en_HK
dc.identifier.issn1027-7811-
dc.identifier.urihttp://hdl.handle.net/10722/106880-
dc.descriptionThis journal issue contain abstracts of the 13th Annual Scientific Meeting of the Institute of Cardiovascular Science and Medicine 2009-
dc.descriptionAbstracts for Posters: P12-
dc.description.abstractBACKGROUND: Mitochondria are the principal source of reactive oxygen species (ROS) in pancreatic islets β-cells and impairment of mitochondrial functions is intrinsically related with diabetes mellitus. Hyperglycemiainduced ROS production by mitochondria is an important aspect in β-cell glucose toxicity. However, most previous studies were performed in either normal islets/single β-cells or insulinoma cells which were bathed in high glucose medium which could not mimic the pathophysiological conditions. OBJECTIVES: To compare and measure hyperglycemia-induced mitochondria ROS generation of primary pancreatic islet β-cells of obese/diabetic (+db/+db) and lean/control (+db/+m) mice, and the effects (acute and chronic) of N-acetyl-L-cysteine (NAC) on ROS generation. METHODS: Collagenase-dissociated single pancreatic islet β-cells of C57BL/KsJ obese/diabetic (+db/+db) mice which exhibit phenotypes of the human T2DM were harvested, and the effects (acute, 10 min; chronic, 24 h) of NAC (20 mM) on high glucose-induced mitochondrial ROS generation were evaluated. Mitochondrial ROS levels were estimated by MitoTracker Red (reduced form) (a selective fluorescence probe for mitochondrial ROS measurement) using con-focal microscope. RESULTS: A trend of, but a non-significant, higher resting/basal ROS level was observed in single pancreatic β-cells of +db/+db mice compared to +db/+m mice. High glucose (15 mM) application gradually caused an increase in ROS levels in single pancreatic β-cells of +db/+db mice whereas no apparent change was observed in +db/+m mice. Chronic (24 h), but not acute (10 min), treatments with NAC (20 mM) ameliorated high-glucose induced ROS generation in single pancreatic β-cells of +db/+db mice. CONCLUSIONS: Hyperglycemia elicited mitochondrial ROS generation only in single pancreatic β-cells of +db/+db mice. Chronic NAC (a well known anti-oxidant) pre-treatment eradicated high glucose-induced ROS generation. Current study is underway to elucidate the underlying mechanism(s) involved in the differential effects of high glucose on ROS generation as well as the identification of the particular mitochondrial ROS generating system.-
dc.languageengen_HK
dc.publisherHong Kong College of Cardiology. The Journal's web site is located at http://www.hkcchk.com/journals.php#3-
dc.relation.ispartofJournal of the Hong Kong College of Cardiologyen_HK
dc.subjectCardiovascular disease-
dc.titleAmelioration of hyperglycemia-induced mitochondrial ROS generation of single pancreatic islet β-cells of obese/diabetic mice by chronic N-Acetyl-L-Cysteineen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailLeung, GPH: gphleung@hkucc.hku.hk-
dc.identifier.authorityKong, SK=rp00557en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.hkuros169829en_HK
dc.identifier.volume17en_HK
dc.identifier.issue2en_HK
dc.identifier.spage59en_HK
dc.identifier.epage59-
dc.publisher.placeHong Kong-

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