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Article: α-Lipoic acid increases cardiac glucose oxidation independent of AMP-activated protein kinase in isolated working rat hearts

Titleα-Lipoic acid increases cardiac glucose oxidation independent of AMP-activated protein kinase in isolated working rat hearts
Authors
Issue Date2007
Citation
Basic Research in Cardiology, 2007, v. 102 n. 5, p. 436-444 How to Cite?
Abstractα-Lipoic acid (ALA) is a naturally occurring enantiomer of lipoic acid and is a cofactor of key metabolic enzyme complexes catalyzing the decarboxylation of α-keto acids. It was recently shown that ALA increases insulin sensitivity by activating AMP-activated protein kinase (AMPK) in skeletal muscle. Also, administration of ALA to obese rats increases insulin-stimulated glucose uptake in the whole body. We investigated the metabolic effects of ALA on isolated working rat hearts. ALA (500μM) stimulated glucose oxidation (157 ± 31 nmol·dry wt-1·min-1 in control vs 315 ± 63 nmoldry wt-1·min-1 in ALA-treated, p < 0.05) without affecting glycolysis, lactate oxidation,or palmitate oxidation.Cardiac work was not affected by ALA treatment. The effect of ALA on glucose oxidation was not associated with an activation of AMPK. AMPK activity was 190 ± 14 pmol · mg protein-1·min-1 in control vs 190±16 pmol·mg protein-1·min-1 in ALAtreated hearts. This study shows that ALA stimulates glucose oxidation in isolated working rat hearts independent of AMPK activation. The beneficial effects of ALA treatment in diabetic patients may be at least in part related to its effect on glucose metabolism. © Steinkopff Verlag 2007.
Persistent Identifierhttp://hdl.handle.net/10722/195875
ISSN
2015 Impact Factor: 6.008
2015 SCImago Journal Rankings: 2.908
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorOnay-Besikci, A-
dc.contributor.authorWagg, C-
dc.contributor.authorLopaschuk, TP-
dc.contributor.authorKeung, W-
dc.contributor.authorLopaschuk, GD-
dc.date.accessioned2014-03-19T01:46:12Z-
dc.date.available2014-03-19T01:46:12Z-
dc.date.issued2007-
dc.identifier.citationBasic Research in Cardiology, 2007, v. 102 n. 5, p. 436-444-
dc.identifier.issn0300-8428-
dc.identifier.urihttp://hdl.handle.net/10722/195875-
dc.description.abstractα-Lipoic acid (ALA) is a naturally occurring enantiomer of lipoic acid and is a cofactor of key metabolic enzyme complexes catalyzing the decarboxylation of α-keto acids. It was recently shown that ALA increases insulin sensitivity by activating AMP-activated protein kinase (AMPK) in skeletal muscle. Also, administration of ALA to obese rats increases insulin-stimulated glucose uptake in the whole body. We investigated the metabolic effects of ALA on isolated working rat hearts. ALA (500μM) stimulated glucose oxidation (157 ± 31 nmol·dry wt-1·min-1 in control vs 315 ± 63 nmoldry wt-1·min-1 in ALA-treated, p < 0.05) without affecting glycolysis, lactate oxidation,or palmitate oxidation.Cardiac work was not affected by ALA treatment. The effect of ALA on glucose oxidation was not associated with an activation of AMPK. AMPK activity was 190 ± 14 pmol · mg protein-1·min-1 in control vs 190±16 pmol·mg protein-1·min-1 in ALAtreated hearts. This study shows that ALA stimulates glucose oxidation in isolated working rat hearts independent of AMPK activation. The beneficial effects of ALA treatment in diabetic patients may be at least in part related to its effect on glucose metabolism. © Steinkopff Verlag 2007.-
dc.languageeng-
dc.relation.ispartofBasic Research in Cardiology-
dc.titleα-Lipoic acid increases cardiac glucose oxidation independent of AMP-activated protein kinase in isolated working rat hearts-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1007/s00395-007-0661-4-
dc.identifier.pmid17530314-
dc.identifier.scopuseid_2-s2.0-34548025597-
dc.identifier.volume102-
dc.identifier.issue5-
dc.identifier.spage436-
dc.identifier.epage444-
dc.identifier.isiWOS:000248894100006-

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