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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
Title | Association between serum amyloid A and scavenger receptor class B type 1-mediated cholesterol efflux to serum in type 2 diabetes |
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Authors | |
Issue Date | 2013 |
Publisher | American Diabetes Association. |
Citation | The 73rd Scientific Sessions of the American Diabetes Association (ADA 2013), Chicago, IL., 21-25 June 2013. How to Cite? |
Abstract | Serum 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. |
Description | Session - Diabetic Dyslipidemia: abstract no. 638-P |
Persistent Identifier | http://hdl.handle.net/10722/186859 |
DC Field | Value | Language |
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dc.contributor.author | Tsun, GS | en_US |
dc.contributor.author | Shiu, SWM | en_US |
dc.contributor.author | Wong, Y | en_US |
dc.contributor.author | Yung, S | en_US |
dc.contributor.author | Chan, TM | en_US |
dc.contributor.author | Tan, KCB | en_US |
dc.date.accessioned | 2013-08-20T12:21:15Z | - |
dc.date.available | 2013-08-20T12:21:15Z | - |
dc.date.issued | 2013 | en_US |
dc.identifier.citation | The 73rd Scientific Sessions of the American Diabetes Association (ADA 2013), Chicago, IL., 21-25 June 2013. | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/186859 | - |
dc.description | Session - Diabetic Dyslipidemia: abstract no. 638-P | - |
dc.description.abstract | Serum 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.language | eng | en_US |
dc.publisher | American Diabetes Association. | - |
dc.relation.ispartof | Scientific Sessions of the American Diabetes Association, ADA 2013 | en_US |
dc.title | Association between serum amyloid A and scavenger receptor class B type 1-mediated cholesterol efflux to serum in type 2 diabetes | en_US |
dc.type | Conference_Paper | en_US |
dc.identifier.email | Shiu, SWM: swmshiu@hku.hk | en_US |
dc.identifier.email | Wong, Y: ywong@hku.hk | en_US |
dc.identifier.email | Yung, S: ssyyung@hku.hk | en_US |
dc.identifier.email | Chan, TM: dtmchan@hku.hk | en_US |
dc.identifier.email | Tan, KCB: kcbtan@hku.hk | en_US |
dc.identifier.authority | Yung, S=rp00455 | en_US |
dc.identifier.authority | Chan, TM=rp00394 | en_US |
dc.identifier.authority | Tan, KCB=rp00402 | en_US |
dc.description.nature | link_to_OA_fulltext | - |
dc.identifier.hkuros | 220913 | en_US |
dc.publisher.place | United States | - |