Renal accumulation of biglycan and lipid retention accelerates diabetic nephropathy

Joel Thompson, Patricia Wilson, Katie Brandewie, Deepa Taneja, Liliana Schaefer, Bonnie Mitchell, Lisa R. Tannock

Research output: Contribution to journalArticlepeer-review

40 Scopus citations


Hyperlipidemia worsens diabetic nephropathy, although the mechanism by which renal lipids accumulate is unknown. We previously demonstrated that renal proteoglycans have high low-density lipoprotein (LDL) binding affinity, suggesting that proteoglycan-mediated LDL retention may contribute to renal lipid accumulation. The aim of this study was to determine the relative effect of diabetes and hyperlipidemia on renal proteoglycan content. Diabetic and non-diabetic LDL receptordeficient mice were fed diets containing 0% or 0.12% cholesterol for 26 weeks, and then kidneys were analyzed for renal lipid and proteoglycan content. Diabetic mice on the high-cholesterol diet had accelerated development of diabetic nephropathy with elevations in urine albumin excretion, glomerular and renal hypertrophy, and mesangial matrix expansion. Renal lipid accumulation was significantly increased by consumption of the 0.12% cholesterol diet, diabetes, and especially by both. The renal proteoglycans biglycan and decorin were detectable in glomeruli, with a significant increase in renal biglycan content in diabetic mice on the high-cholesterol diet. Renal biglycan and renal apolipoprotein B were colocalized, and regression analyses showed a significant relation between renal biglycan and renal apolipoprotein B content. The increased renal biglycan content in diabetic nephropathy probably contributes to renal lipid accumulation and the development of diabetic nephropathy.

Original languageEnglish
Pages (from-to)1179-1187
Number of pages9
JournalAmerican Journal of Pathology
Issue number3
StatePublished - Sep 2011

ASJC Scopus subject areas

  • Pathology and Forensic Medicine


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