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Conference Paper: Association between serum amyloid A and scavenger receptor class B type 1-mediated cholesterol efflux to serum in type 2 diabetes

TitleAssociation between serum amyloid A and scavenger receptor class B type 1-mediated cholesterol efflux to serum in type 2 diabetes
Authors
Issue Date2013
PublisherAmerican Diabetes Association.
Citation
The 73rd Scientific Sessions of the American Diabetes Association, Chicago, IL., 21-25 June 2013. How to Cite?
AbstractSerum amyloid A (SAA) is an acute phase response protein and has apolipoprotein properties. Recent evidence from animal studies has shown that SAA impairs reverse cholesterol transport during the acute phase response in vivo. Since type 2 diabetes is associated with chronic subclinical inflammation, the objective is to investigate the changes in SAA level in type 2 diabetic patients and to evaluate the relationship between SAA and the capacity of serum to induce cellular cholesterol efflux via the two known cholesterol transporters, scavenger receptor class B type I (SR-BI) and adenosine triphosphate binding cassette transporter G1 (ABCG1). 264 diabetic patients not on lipid lowering agents and 275 non-diabetic controls were recruited. Diabetic patients were subdivided into those with normoalbuminuria (NA, n=110), microalbuminuria (MA, n=79) and proteinuria (P, n=75). SAA was measured by ELISA. SR-BI-mediated and ABCG1-mediated cholesterol efflux to serum was determined by measuring the transfer of [3H]cholesterol from Fu5AH rat hepatoma cells expressing SR-BI and from human ABCG1-transfected CHO-K1 cells to the medium containing the tested serum respectively. SAA was increased in MA and P (p<0.01) compared to controls. Both SR-BI-mediated and ABCG1-mediated cholesterol efflux to serum was significantly impaired in all 3 groups of diabetic patients (p<0.01) with the proteinuric group having the largest magnitude of reduction. These changes remained significant even after adjusting for plasma HDL-C level. SAA inversely correlated with SR-BI-mediated cholesterol efflux (r=-0.36, p<0.01) but not with ABCG1-mediated cholesterol efflux. On linear regression analysis, plasma HDL-C, SAA and eGFR were independent determinants of SR-BI-mediated cholesterol efflux. SAA was increased in type 2 diabetic patients with incipient or overt nephropathy and associated with impairment of SR-BI-mediated cholesterol efflux to serum.
DescriptionSession - Diabetic Dyslipidemia: abstract no. 638-P
Persistent Identifierhttp://hdl.handle.net/10722/186859

 

DC FieldValueLanguage
dc.contributor.authorTsun, GSen_US
dc.contributor.authorShiu, SWMen_US
dc.contributor.authorWong, Yen_US
dc.contributor.authorYung, Sen_US
dc.contributor.authorChan, TMen_US
dc.contributor.authorTan, KCBen_US
dc.date.accessioned2013-08-20T12:21:15Z-
dc.date.available2013-08-20T12:21:15Z-
dc.date.issued2013en_US
dc.identifier.citationThe 73rd Scientific Sessions of the American Diabetes Association, Chicago, IL., 21-25 June 2013.en_US
dc.identifier.urihttp://hdl.handle.net/10722/186859-
dc.descriptionSession - Diabetic Dyslipidemia: abstract no. 638-P-
dc.description.abstractSerum amyloid A (SAA) is an acute phase response protein and has apolipoprotein properties. Recent evidence from animal studies has shown that SAA impairs reverse cholesterol transport during the acute phase response in vivo. Since type 2 diabetes is associated with chronic subclinical inflammation, the objective is to investigate the changes in SAA level in type 2 diabetic patients and to evaluate the relationship between SAA and the capacity of serum to induce cellular cholesterol efflux via the two known cholesterol transporters, scavenger receptor class B type I (SR-BI) and adenosine triphosphate binding cassette transporter G1 (ABCG1). 264 diabetic patients not on lipid lowering agents and 275 non-diabetic controls were recruited. Diabetic patients were subdivided into those with normoalbuminuria (NA, n=110), microalbuminuria (MA, n=79) and proteinuria (P, n=75). SAA was measured by ELISA. SR-BI-mediated and ABCG1-mediated cholesterol efflux to serum was determined by measuring the transfer of [3H]cholesterol from Fu5AH rat hepatoma cells expressing SR-BI and from human ABCG1-transfected CHO-K1 cells to the medium containing the tested serum respectively. SAA was increased in MA and P (p<0.01) compared to controls. Both SR-BI-mediated and ABCG1-mediated cholesterol efflux to serum was significantly impaired in all 3 groups of diabetic patients (p<0.01) with the proteinuric group having the largest magnitude of reduction. These changes remained significant even after adjusting for plasma HDL-C level. SAA inversely correlated with SR-BI-mediated cholesterol efflux (r=-0.36, p<0.01) but not with ABCG1-mediated cholesterol efflux. On linear regression analysis, plasma HDL-C, SAA and eGFR were independent determinants of SR-BI-mediated cholesterol efflux. SAA was increased in type 2 diabetic patients with incipient or overt nephropathy and associated with impairment of SR-BI-mediated cholesterol efflux to serum.-
dc.languageengen_US
dc.publisherAmerican Diabetes Association.-
dc.relation.ispartof73rd Scientific Sessions of the American Diabetes Association 2013en_US
dc.titleAssociation between serum amyloid A and scavenger receptor class B type 1-mediated cholesterol efflux to serum in type 2 diabetesen_US
dc.typeConference_Paperen_US
dc.identifier.emailShiu, SWM: swmshiu@hku.hken_US
dc.identifier.emailWong, Y: ywong@hku.hken_US
dc.identifier.emailYung, S: ssyyung@hku.hken_US
dc.identifier.emailChan, TM: dtmchan@hku.hken_US
dc.identifier.emailTan, KCB: kcbtan@hku.hken_US
dc.identifier.authorityYung, S=rp00455en_US
dc.identifier.authorityChan, TM=rp00394en_US
dc.identifier.authorityTan, KCB=rp00402en_US
dc.description.naturelink_to_OA_fulltext-
dc.identifier.hkuros220913en_US
dc.publisher.placeUnited States-

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