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Publication
Genetic modulation of diabetic nephropathy among mouse strains with Ins2 Akita
mutation.
Authors
Wu X, Davis RC, McMillen TS, Schaeffer V, Zhou Z, Qi H, Mazandarani PN, Alialy
R, Hudkins KL, Lusis AJ, LeBoeuf RC
Submitted By
Submitted Externally on 12/8/2014
Status
Published
Journal
Physiological reports
Year
2014
Date Published
11/1/2014
Volume : Pages
2 :
Not Specified
PubMed Reference
25428948
Abstract
Diabetic nephropathy (DN) is a major complication of diabetes and the leading
cause of end-stage renal disease. DN is characterized by changes in kidney
structure and function but the underlying genetic and molecular factors are
poorly understood. We used a mouse diversity panel to explore the genetic basis
of DN traits in mice carrying the Ins2 Akita mutation. Twenty-eight Akita
strains were generated by breeding this panel to DBA/2.Akita mice. Male F1
diabetic and nondiabetic littermates were evaluated for DN-related traits. Urine
albumin-to-creatinine ratios (ACRs), volume and cystatin C as well as blood urea
nitrogen and lipoprotein levels varied significantly among the diabetic strains.
For most Akita strains, ACR values increased 2- to 6-fold over euglycemic
control values. However, six strains exhibited changes in ACR exceeding 10-fold
with two strains (NOD/ShiLt and CBA) showing 50- to 83- fold increases. These
increases are larger than previously reported among available DN mouse models
establishing these strains as useful for additional studies of renal function.
ACRs correlated with cystatin C (P = 0.0286), a measure of hyperfiltration and
an interstitial tubular marker associated with DN onset in humans suggesting
that tubule damage as well as podocyte-stress contributed to reduced kidney
function assessed by ACR. Although large changes were seen for ACRs, severe
nephropathology was absent. However, glomerular hypertrophy and collagen IV
content were found to vary significantly among strains suggesting a genetic
basis for early onset features of DN. Our results define the range of DN
phenotypes that occur among common inbred strains of mice.
Investigators with authorship
Name
Institution
Richard Davis
University of California Los Angeles
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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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