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Conference Paper: Cholesterol transport proteins and diabetic nephropathy

TitleCholesterol transport proteins and diabetic nephropathy
Authors
Issue Date2013
PublisherThe International Diabetes Federation (IDF).
Citation
The World Diabetes Congress (WDC), Melbourne, Australia, 2-6 December 2013, abstract no. PD-0703 How to Cite?
AbstractAims: Lipid accumulation in the kidney has been shown to accelerate renal injury. Intracellular accumulation of lipids may be caused by alterations in synthesis as well as lipid uptake and efflux. Cellular cholesterol efflux is mediated by specific cholesterol transport proteins including scavenger receptor class B type 1 (SR-BI), adenosine triphosphate binding cassette transporter G1 (ABCG1) and ABCA1. We have investigated whether there are changes in cellular cholesterol transport proteins in diabetic nephropathy. Methods: Protein expression of SR-BI, ABCG1 and ABCA1 was determined in human mesangial cells and tubular cells cultured under normal or high glucose conditions in vitro. Renal expression of these cholesterol transporters was examined in mice with streptozotocin-induced type 1 diabetes. Results: SR-BI, ABCG1 and ABCA1 were expressed in both human mesangial cells and tubular cells. Incubation of mesangial cells and tubular cells with HDL stimulated cellular cholesterol efflux by 2.7 ± 0.2 fold, p<0.01 and 2.1 ± 0.3 fold, p<0.05 respectively, whereas incubation with apolipoprotein A1 had a lesser effect. In vitro, hyperglycemia significantly reduced the expression of all three cholesterol transporters in a dose-dependent manner. In vivo studies showed that renal cholesterol (1.5 ± 0.2 fold, p<0.01) and triglyceride content (2.9 ± 0.2 fold, p<0.01) was increased in diabetic mice with nephropathy compared to non-diabetic control mice. This was associated with a significant reduction in the protein expression of ABCA1 (59 ± 16%, p<0.05), ABCG1 (73 ± 14%, p<0.05) and SR-BI (58 ± 10%, p<0.01) in the kidneys. Glomerular abnormalities and tubulo-interstitial changes were noted in mice with diabetic nephropathy and immunohistological examination showed that there was a marked reduction in all three cholesterol transporters particularly in the renal tubules. Conclusion: Reduced renal expression of SR-BI, ABCG1 and ABCA1 was associated with diabetic nephropathy. Defects in cholesterol export pathway in renal cells could promote cholesterol accumulation and might contribute to the development of diabetic nephropathy. Acknowledgement: supported by funding from the Hong Kong Research Grants Council Research Fund (HKU 776709M). No conflict of interest
DescriptionSession: Renal - clinical
Persistent Identifierhttp://hdl.handle.net/10722/201280

 

DC FieldValueLanguage
dc.contributor.authorTan, KCBen_US
dc.contributor.authorTsun, GSen_US
dc.contributor.authorYung, SSYen_US
dc.contributor.authorChau, KMen_US
dc.contributor.authorShiu, SWMen_US
dc.contributor.authorChan, DTMen_US
dc.date.accessioned2014-08-21T07:20:17Z-
dc.date.available2014-08-21T07:20:17Z-
dc.date.issued2013en_US
dc.identifier.citationThe World Diabetes Congress (WDC), Melbourne, Australia, 2-6 December 2013, abstract no. PD-0703en_US
dc.identifier.urihttp://hdl.handle.net/10722/201280-
dc.descriptionSession: Renal - clinical-
dc.description.abstractAims: Lipid accumulation in the kidney has been shown to accelerate renal injury. Intracellular accumulation of lipids may be caused by alterations in synthesis as well as lipid uptake and efflux. Cellular cholesterol efflux is mediated by specific cholesterol transport proteins including scavenger receptor class B type 1 (SR-BI), adenosine triphosphate binding cassette transporter G1 (ABCG1) and ABCA1. We have investigated whether there are changes in cellular cholesterol transport proteins in diabetic nephropathy. Methods: Protein expression of SR-BI, ABCG1 and ABCA1 was determined in human mesangial cells and tubular cells cultured under normal or high glucose conditions in vitro. Renal expression of these cholesterol transporters was examined in mice with streptozotocin-induced type 1 diabetes. Results: SR-BI, ABCG1 and ABCA1 were expressed in both human mesangial cells and tubular cells. Incubation of mesangial cells and tubular cells with HDL stimulated cellular cholesterol efflux by 2.7 ± 0.2 fold, p<0.01 and 2.1 ± 0.3 fold, p<0.05 respectively, whereas incubation with apolipoprotein A1 had a lesser effect. In vitro, hyperglycemia significantly reduced the expression of all three cholesterol transporters in a dose-dependent manner. In vivo studies showed that renal cholesterol (1.5 ± 0.2 fold, p<0.01) and triglyceride content (2.9 ± 0.2 fold, p<0.01) was increased in diabetic mice with nephropathy compared to non-diabetic control mice. This was associated with a significant reduction in the protein expression of ABCA1 (59 ± 16%, p<0.05), ABCG1 (73 ± 14%, p<0.05) and SR-BI (58 ± 10%, p<0.01) in the kidneys. Glomerular abnormalities and tubulo-interstitial changes were noted in mice with diabetic nephropathy and immunohistological examination showed that there was a marked reduction in all three cholesterol transporters particularly in the renal tubules. Conclusion: Reduced renal expression of SR-BI, ABCG1 and ABCA1 was associated with diabetic nephropathy. Defects in cholesterol export pathway in renal cells could promote cholesterol accumulation and might contribute to the development of diabetic nephropathy. Acknowledgement: supported by funding from the Hong Kong Research Grants Council Research Fund (HKU 776709M). No conflict of interest-
dc.languageengen_US
dc.publisherThe International Diabetes Federation (IDF).-
dc.relation.ispartofWorld Diabetes Congressen_US
dc.titleCholesterol transport proteins and diabetic nephropathyen_US
dc.typeConference_Paperen_US
dc.identifier.emailTan, KCB: kcbtan@hku.hken_US
dc.identifier.emailYung, SSY: ssyyung@hku.hken_US
dc.identifier.emailChau, KM: melchau@hkucc.hku.hken_US
dc.identifier.emailShiu, SWM: swmshiu@hku.hken_US
dc.identifier.emailChan, DTM: dtmchan@hku.hken_US
dc.identifier.authorityTan, KCB=rp00402en_US
dc.identifier.authorityYung, SSY=rp00455en_US
dc.identifier.authorityChan, DTM=rp00394en_US
dc.identifier.hkuros234418en_US

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