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Publication
Reduced expression of lipoic acid synthase accelerates diabetic nephropathy.
Authors
Yi X, Xu L, Hiller S, Kim HS, Nickeleit V, James LR, Maeda N
Submitted By
Nobuyo Maeda on 2/22/2012
Status
Published
Journal
Journal of the American Society of Nephrology : JASN
Year
2012
Date Published
1/1/2012
Volume : Pages
23 : 103 - 111
PubMed Reference
22021711
Abstract
Oxidative stress contributes to the pathogenesis of diabetic nephropathy. In
mitochondria, lipoic acid synthase produces a-lipoic acid, an antioxidant and an
essential cofactor in a-ketoacid dehydrogenase complexes, which participate in
glucose oxidation and ATP generation. Administration of lipoic acid abrogates
diabetic nephropathy in animal models, but whether lower production of
endogenous lipoic acid promotes diabetic nephropathy is unknown. Here, we
crossed mice heterozygous for lipoic acid synthase deficiency (Lias(+/-)) with
Ins2(Akita/+) mice, a well characterized model of type 1 diabetes. Double mutant
mice had more overt diabetic nephropathy, including microalbuminuria, glomerular
basement thickening, mesangial matrix expansion, and hypertension, compared with
Lias(+/+)Ins2(Akita/+) controls. We also identified proximal tubules as a major
site for generation of superoxide anions during diabetic nephropathy.
Mitochondria in proximal tubular cells were particularly sensitive to damage in
diabetic mice with reduced lipoic acid production. These results suggest that
lipoic acid synthase deficiency increases oxidative stress and accelerates the
development of diabetic nephropathy.
Investigators with authorship
Name
Institution
Nobuyo Maeda
University of North Carolina
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Please acknowledge all posters, manuscripts or scientific materials that were generated in part or whole using funds from the Diabetic Complications Consortium(DiaComp) using the following text:
Financial support for this work provided by the NIDDK Diabetic Complications Consortium (RRID:SCR_001415, www.diacomp.org), grants DK076169 and DK115255
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