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Article: Intracerebroventricular leptin administration differentially alters cardiac energy metabolism in mice fed a low-fat and high-fat diet

TitleIntracerebroventricular leptin administration differentially alters cardiac energy metabolism in mice fed a low-fat and high-fat diet
Authors
Issue Date2011
Citation
Journal of Cardiovascular Pharmacology, 2011, v. 57 n. 1, p. 103-113 How to Cite?
AbstractLeptin directly acts on peripheral tissues and alters energy metabolism in obese mice. It also has acute beneficial effects on these tissues via its hypothalamic action. However, it is not clear what effect chronic intracerebroventrical (ICV) leptin administration has on cardiac energy metabolism. We examined the effects of chronic ICV leptin on glucose and fatty acid metabolism in isolated working hearts from high-fat-fed and low-fat-fed mice. Mice were fed a high-fat (60% calories from fat) or low-fat (10% calories from fat) diet for 8 weeks before ICV leptin (5 μg/d) for 7 days. In low-fat-fed mice, leptin increased glucose oxidation rates in isolated working hearts when compared with control [203 ± 21 vs. 793 ± 93 nmol•(g dry weight)•min]. In high-fat-fed mice leptin inhibited fatty acid oxidation [476 ± 73 vs. 251 ± 38 nmol•(g•dry• wt)•min]. The increase in glucose oxidation in low-fat-fed mice was accompanied by increased pyruvate dehydrogenase activity. In high-fat-fed mice, leptin increased cardiac malonyl coenzyme A levels, secondary to a decrease in malonyl coenzyme A decarboxylase expression. These results suggest that ICV leptin alters cardiac energy metabolism opposite to its peripheral effects and that these effects differ depending on energy substrate supply to the mice. Copyright © 2011 by Lippincott Williams & Wilkins.
Persistent Identifierhttp://hdl.handle.net/10722/195859
ISSN
2015 Impact Factor: 2.462
2015 SCImago Journal Rankings: 0.962
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorKeung, W-
dc.contributor.authorCadete, VJJ-
dc.contributor.authorPalaniyappan, A-
dc.contributor.authorJablonski, A-
dc.contributor.authorFischer, M-
dc.contributor.authorLopaschuk, GD-
dc.date.accessioned2014-03-19T01:46:10Z-
dc.date.available2014-03-19T01:46:10Z-
dc.date.issued2011-
dc.identifier.citationJournal of Cardiovascular Pharmacology, 2011, v. 57 n. 1, p. 103-113-
dc.identifier.issn0160-2446-
dc.identifier.urihttp://hdl.handle.net/10722/195859-
dc.description.abstractLeptin directly acts on peripheral tissues and alters energy metabolism in obese mice. It also has acute beneficial effects on these tissues via its hypothalamic action. However, it is not clear what effect chronic intracerebroventrical (ICV) leptin administration has on cardiac energy metabolism. We examined the effects of chronic ICV leptin on glucose and fatty acid metabolism in isolated working hearts from high-fat-fed and low-fat-fed mice. Mice were fed a high-fat (60% calories from fat) or low-fat (10% calories from fat) diet for 8 weeks before ICV leptin (5 μg/d) for 7 days. In low-fat-fed mice, leptin increased glucose oxidation rates in isolated working hearts when compared with control [203 ± 21 vs. 793 ± 93 nmol•(g dry weight)•min]. In high-fat-fed mice leptin inhibited fatty acid oxidation [476 ± 73 vs. 251 ± 38 nmol•(g•dry• wt)•min]. The increase in glucose oxidation in low-fat-fed mice was accompanied by increased pyruvate dehydrogenase activity. In high-fat-fed mice, leptin increased cardiac malonyl coenzyme A levels, secondary to a decrease in malonyl coenzyme A decarboxylase expression. These results suggest that ICV leptin alters cardiac energy metabolism opposite to its peripheral effects and that these effects differ depending on energy substrate supply to the mice. Copyright © 2011 by Lippincott Williams & Wilkins.-
dc.languageeng-
dc.relation.ispartofJournal of Cardiovascular Pharmacology-
dc.titleIntracerebroventricular leptin administration differentially alters cardiac energy metabolism in mice fed a low-fat and high-fat diet-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1097/FJC.0b013e31820014f9-
dc.identifier.pmid20980918-
dc.identifier.scopuseid_2-s2.0-78951481202-
dc.identifier.hkuros239610-
dc.identifier.volume57-
dc.identifier.issue1-
dc.identifier.spage103-
dc.identifier.epage113-
dc.identifier.isiWOS:000286178000014-

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