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Conference Paper: Effects of cigarette smoke exposure on adiponectin levels in rats

TitleEffects of cigarette smoke exposure on adiponectin levels in rats
Authors
Issue Date2009
PublisherHong Kong Academy of Medicine Press. The Journal's web site is located at http://www.hkmj.org/
Citation
The 14th Medical Research Conference, Department of Medicine, The University of Hong Kong, Hong Kong, 10 January 2009. In Hong Kong Medical Journal, 2009, v. 15 n. Supp 1, p. 28 How to Cite?
AbstractIntroduction: Adiponectin, a member of the adipokine family, is a 247-amino acid protein mainly secreted by adipocytes and plays an important role in lipid metabolism and glucose homeostasis. Unlike many adipokines, plasma levels of adiponectin are significantly decreased in the obese, patients with diabetes, hypertension, dislipidaemia, or ischaemic heart disease compared with healthy individuals. Recently, cigarette smoke (CS) has been found to cause a decline in human serum adiponectin levels. The current study was undertaken to investigate circulating adiponectin level over time in an in-vivo experimental rat model after CS exposure. Methods: Sprague-Dawley rats were randomly divided into two groups, ie sham air and 4% CS for a period of 7, 28, and 56 days. Exposure to sham air or 4% CS was performed for 1 hour/day in the ventilated smoking chamber. At the end of each time-point 24 hours after last exposure of CS, the animals were sacrificed. Serum and bronchoalveolar lavage fluid (BALF) were collected and analysed for adiponectin using in-house ELISA kits. Results: Serum adiponectin levels were significantly decreased after 28-day (2885±361 vs 4841±557 ng/mL; n=10) and after 56-day (2537±321 vs 3771±460 ng/mL) but not after 7-day CS exposure (4772±694 vs 5838±654 ng/mL). In BALF, CS-induced reduction in adiponectin levels was also observed in comparison to sham-air group after 56 days (6.5±2.9 vs 42.3±19.9 ng/mL; n=5). Adiponectin was present with higher concentration in serum than in BALF. CS group showed a lower body weight gain over time than did SA group despite similar body weight at baseline. Conclusion: We revealed that smoking exposure for a limited period of time was associated with low adiponectin level. The present finding may provide evidence of the importance of a causal relationship between smoking and adiponectin concentrations. Further studies will be required to elucidate the mechanism of CS on the regulation of adiponectin in circulation and in lung. Acknowledgement: This research was supported by Hong Kong Lung Foundation Research Grant.
Persistent Identifierhttp://hdl.handle.net/10722/62310
ISSN
2015 Impact Factor: 0.887
2015 SCImago Journal Rankings: 0.279

 

DC FieldValueLanguage
dc.contributor.authorMak, JCW-
dc.contributor.authorChan, KH-
dc.contributor.authorXu, A-
dc.contributor.authorHo, SP-
dc.contributor.authorMan, RYK-
dc.contributor.authorLam, KSL-
dc.contributor.authorIp, MSM-
dc.date.accessioned2010-07-13T03:58:32Z-
dc.date.available2010-07-13T03:58:32Z-
dc.date.issued2009-
dc.identifier.citationThe 14th Medical Research Conference, Department of Medicine, The University of Hong Kong, Hong Kong, 10 January 2009. In Hong Kong Medical Journal, 2009, v. 15 n. Supp 1, p. 28-
dc.identifier.issn1024-2708-
dc.identifier.urihttp://hdl.handle.net/10722/62310-
dc.description.abstractIntroduction: Adiponectin, a member of the adipokine family, is a 247-amino acid protein mainly secreted by adipocytes and plays an important role in lipid metabolism and glucose homeostasis. Unlike many adipokines, plasma levels of adiponectin are significantly decreased in the obese, patients with diabetes, hypertension, dislipidaemia, or ischaemic heart disease compared with healthy individuals. Recently, cigarette smoke (CS) has been found to cause a decline in human serum adiponectin levels. The current study was undertaken to investigate circulating adiponectin level over time in an in-vivo experimental rat model after CS exposure. Methods: Sprague-Dawley rats were randomly divided into two groups, ie sham air and 4% CS for a period of 7, 28, and 56 days. Exposure to sham air or 4% CS was performed for 1 hour/day in the ventilated smoking chamber. At the end of each time-point 24 hours after last exposure of CS, the animals were sacrificed. Serum and bronchoalveolar lavage fluid (BALF) were collected and analysed for adiponectin using in-house ELISA kits. Results: Serum adiponectin levels were significantly decreased after 28-day (2885±361 vs 4841±557 ng/mL; n=10) and after 56-day (2537±321 vs 3771±460 ng/mL) but not after 7-day CS exposure (4772±694 vs 5838±654 ng/mL). In BALF, CS-induced reduction in adiponectin levels was also observed in comparison to sham-air group after 56 days (6.5±2.9 vs 42.3±19.9 ng/mL; n=5). Adiponectin was present with higher concentration in serum than in BALF. CS group showed a lower body weight gain over time than did SA group despite similar body weight at baseline. Conclusion: We revealed that smoking exposure for a limited period of time was associated with low adiponectin level. The present finding may provide evidence of the importance of a causal relationship between smoking and adiponectin concentrations. Further studies will be required to elucidate the mechanism of CS on the regulation of adiponectin in circulation and in lung. Acknowledgement: This research was supported by Hong Kong Lung Foundation Research Grant.-
dc.languageeng-
dc.publisherHong Kong Academy of Medicine Press. The Journal's web site is located at http://www.hkmj.org/-
dc.relation.ispartofHong Kong Medical Journal-
dc.rightsHong Kong Medical Journal. Copyright © Hong Kong Academy of Medicine Press.-
dc.titleEffects of cigarette smoke exposure on adiponectin levels in rats-
dc.typeConference_Paper-
dc.identifier.emailMak, JCW: judymak@HKUCC.hku.hk-
dc.identifier.emailXu, A: amxu@hkucc.hku.hk-
dc.identifier.emailMan, RYK: rykman@hkucc.hku.hk-
dc.identifier.emailLam, KSL: ksllam@hku.hk-
dc.identifier.emailIp, MSM: msmip@hku.hk-
dc.identifier.authorityMak, JCW=rp00352-
dc.identifier.authorityXu, A=rp00485-
dc.identifier.authorityMan, RYK=rp00236-
dc.identifier.authorityLam, KSL=rp00343-
dc.identifier.authorityIp, MSM=rp00347-
dc.identifier.hkuros162751-
dc.identifier.volume15-
dc.identifier.issueSupp 1-
dc.identifier.spage28-
dc.identifier.epage28-
dc.publisher.placeHong Kong-

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