Cholesterol Contributes to Diabetic Nephropathy through SCAP-SREBP-2 Pathway

Diabetic nephropathy (DN) has been associated with the presence of lipid deposition. We hypothesized that the disruption of intracellular cholesterol feedback may contribute to DN. Diabetes was induced by high fat/sucrose diet and low-dose intraperitoneal injection of streptozocin (STZ) in male Spra...

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Main Authors: Hong Sun, Yang Yuan, Zi-Lin Sun
Format: Article
Language:English
Published: Wiley 2013-01-01
Series:International Journal of Endocrinology
Online Access:http://dx.doi.org/10.1155/2013/592576
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author Hong Sun
Yang Yuan
Zi-Lin Sun
author_facet Hong Sun
Yang Yuan
Zi-Lin Sun
author_sort Hong Sun
collection DOAJ
description Diabetic nephropathy (DN) has been associated with the presence of lipid deposition. We hypothesized that the disruption of intracellular cholesterol feedback may contribute to DN. Diabetes was induced by high fat/sucrose diet and low-dose intraperitoneal injection of streptozocin (STZ) in male Sprague-Dawley rats. Then diabetic rats were randomly divided into two groups: untreated diabetic group (DM) and atorvastatin-treated group (DM + AT). We found that the levels of serum blood urea nitrogen and creatinine, as well as 24-hour urine protein and urinary neutrophil gelatinase-associated lipocalin, were significantly increased in diabetic rats. This result indicated that the diabetic rats suffered from functional renal damage. We also observed lipid droplet accumulation and increase in 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMG-CoAR), low density lipoprotein receptor (LDLr), sterol regulatory element binding protein-2 (SREBP-2), and SREBP-cleavage activating protein (SCAP) in the kidneys of diabetic rats. However, atorvastatin ameliorated renal lipid accumulation and improved the renal function of diabetic rats despite an increase in mRNA and protein expressions of HMG-CoAR, LDLr, and SREBP-2. These results demonstrated that intracellular cholesterol feedback regulation is disrupted in rats with type 2 diabetes, thereby causing renal cholesterol accumulation. Atorvastatin ameliorated renal cholesterol accumulation by reducing renal cholesterol synthesis.
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spelling doaj-art-aff7c452d75e44a0a9030178cf2a4ab92025-08-20T03:39:15ZengWileyInternational Journal of Endocrinology1687-83371687-83452013-01-01201310.1155/2013/592576592576Cholesterol Contributes to Diabetic Nephropathy through SCAP-SREBP-2 PathwayHong Sun0Yang Yuan1Zi-Lin Sun2Department of Endocrinology, Zhongda Hospital, Institute of Diabetes, Medical School, Southeast University, Nanjing 210009, ChinaDepartment of Endocrinology, Zhongda Hospital, Institute of Diabetes, Medical School, Southeast University, Nanjing 210009, ChinaDepartment of Endocrinology, Zhongda Hospital, Institute of Diabetes, Medical School, Southeast University, Nanjing 210009, ChinaDiabetic nephropathy (DN) has been associated with the presence of lipid deposition. We hypothesized that the disruption of intracellular cholesterol feedback may contribute to DN. Diabetes was induced by high fat/sucrose diet and low-dose intraperitoneal injection of streptozocin (STZ) in male Sprague-Dawley rats. Then diabetic rats were randomly divided into two groups: untreated diabetic group (DM) and atorvastatin-treated group (DM + AT). We found that the levels of serum blood urea nitrogen and creatinine, as well as 24-hour urine protein and urinary neutrophil gelatinase-associated lipocalin, were significantly increased in diabetic rats. This result indicated that the diabetic rats suffered from functional renal damage. We also observed lipid droplet accumulation and increase in 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMG-CoAR), low density lipoprotein receptor (LDLr), sterol regulatory element binding protein-2 (SREBP-2), and SREBP-cleavage activating protein (SCAP) in the kidneys of diabetic rats. However, atorvastatin ameliorated renal lipid accumulation and improved the renal function of diabetic rats despite an increase in mRNA and protein expressions of HMG-CoAR, LDLr, and SREBP-2. These results demonstrated that intracellular cholesterol feedback regulation is disrupted in rats with type 2 diabetes, thereby causing renal cholesterol accumulation. Atorvastatin ameliorated renal cholesterol accumulation by reducing renal cholesterol synthesis.http://dx.doi.org/10.1155/2013/592576
spellingShingle Hong Sun
Yang Yuan
Zi-Lin Sun
Cholesterol Contributes to Diabetic Nephropathy through SCAP-SREBP-2 Pathway
International Journal of Endocrinology
title Cholesterol Contributes to Diabetic Nephropathy through SCAP-SREBP-2 Pathway
title_full Cholesterol Contributes to Diabetic Nephropathy through SCAP-SREBP-2 Pathway
title_fullStr Cholesterol Contributes to Diabetic Nephropathy through SCAP-SREBP-2 Pathway
title_full_unstemmed Cholesterol Contributes to Diabetic Nephropathy through SCAP-SREBP-2 Pathway
title_short Cholesterol Contributes to Diabetic Nephropathy through SCAP-SREBP-2 Pathway
title_sort cholesterol contributes to diabetic nephropathy through scap srebp 2 pathway
url http://dx.doi.org/10.1155/2013/592576
work_keys_str_mv AT hongsun cholesterolcontributestodiabeticnephropathythroughscapsrebp2pathway
AT yangyuan cholesterolcontributestodiabeticnephropathythroughscapsrebp2pathway
AT zilinsun cholesterolcontributestodiabeticnephropathythroughscapsrebp2pathway