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Genetic modulation of diabetic nephropathy among mouse strains with Ins2 Akita mutation.

Wu X, Davis RC, McMillen TS, Schaeffer V, Zhou Z, Qi H, Mazandarani PN, Alialy R, Hudkins KL, Lusis AJ, LeBoeuf RC - Physiol Rep (2014)

Bottom Line: 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.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.However, glomerular hypertrophy and collagen IV content were found to vary significantly among strains suggesting a genetic basis for early onset features of DN.

View Article: PubMed Central - PubMed

Affiliation: Division of Cardiology, Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California, USA.

No MeSH data available.


Related in: MedlinePlus

Albuminuria (1A), polyuria (1B), blood urea nitrogen (1C), plasma glucose (3A), plasma insulin (3B), plasma triglycerides (3C), left kidney weight (4A), urine cystatin‐C to creatinine ratio (CCR) (4B), urine nephrin to creatinine ratio (4C), glomerular area (5A), and percent glomerular area staining for collagen IV (5B) for diabetic and nondiabetic control mice across a panel of 28 F1 mouse strains. Panel labels show correspondence with panels in Figures 1, 3–5. For each phenotype, strains are shown in alphabetical order by strain in order to facilitate trait‐trait comparisons across strains. Gray bars show control mice and black bars show diabetic mice. Error bars indicate SEM.
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fig07: Albuminuria (1A), polyuria (1B), blood urea nitrogen (1C), plasma glucose (3A), plasma insulin (3B), plasma triglycerides (3C), left kidney weight (4A), urine cystatin‐C to creatinine ratio (CCR) (4B), urine nephrin to creatinine ratio (4C), glomerular area (5A), and percent glomerular area staining for collagen IV (5B) for diabetic and nondiabetic control mice across a panel of 28 F1 mouse strains. Panel labels show correspondence with panels in Figures 1, 3–5. For each phenotype, strains are shown in alphabetical order by strain in order to facilitate trait‐trait comparisons across strains. Gray bars show control mice and black bars show diabetic mice. Error bars indicate SEM.

Mentions: Albuminuria, polyuria and blood urea nitrogen for diabetic and nondiabetic control mice across a panel of 28 F1 mouse strains. To test the impact of genetic background on traits associated with DN, DBA/2.Akita male mice were bred to females of 28 different inbred lines and the resulting male F1 animals were evaluated. F1 animals inheriting the Akita mutation are labeled as diabetic while offspring without the mutation are used as normoglycemic controls. The variation in genetic background as determined by the maternal strain is indicated on the horizontal axis for each graph. For each phenotype, strains are shown in rank order according to strain‐values for that phenotype in diabetic mice. Gray bars show control mice and black bars show diabetic mice. Error bars indicate SEM. (A) Albumin‐to‐creatinine ratios (ACRs, μg urinary albumin per mg urinary creatinine) varied widely among the strains and were elevated for diabetic versus nondiabetic controls in most cases (n = 4–17 mice/group). Nearly all strains showed significant increases in ACR with diabetes (P < 0.001–0.050). (B) Average urine volume (mL per 24 h). Severe polyuria is seen for diabetic as compared to nondiabetic mice. (C) Blood urea nitrogen (BUN) levels (mg/dL). *P < 0.05, n = 4–17. To facilitate comparisons among strains, these data are presented in alphabetical strain order in Figure 7‐1A, 1B and 1C at the end of the manuscript.


Genetic modulation of diabetic nephropathy among mouse strains with Ins2 Akita mutation.

Wu X, Davis RC, McMillen TS, Schaeffer V, Zhou Z, Qi H, Mazandarani PN, Alialy R, Hudkins KL, Lusis AJ, LeBoeuf RC - Physiol Rep (2014)

Albuminuria (1A), polyuria (1B), blood urea nitrogen (1C), plasma glucose (3A), plasma insulin (3B), plasma triglycerides (3C), left kidney weight (4A), urine cystatin‐C to creatinine ratio (CCR) (4B), urine nephrin to creatinine ratio (4C), glomerular area (5A), and percent glomerular area staining for collagen IV (5B) for diabetic and nondiabetic control mice across a panel of 28 F1 mouse strains. Panel labels show correspondence with panels in Figures 1, 3–5. For each phenotype, strains are shown in alphabetical order by strain in order to facilitate trait‐trait comparisons across strains. Gray bars show control mice and black bars show diabetic mice. Error bars indicate SEM.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4255814&req=5

fig07: Albuminuria (1A), polyuria (1B), blood urea nitrogen (1C), plasma glucose (3A), plasma insulin (3B), plasma triglycerides (3C), left kidney weight (4A), urine cystatin‐C to creatinine ratio (CCR) (4B), urine nephrin to creatinine ratio (4C), glomerular area (5A), and percent glomerular area staining for collagen IV (5B) for diabetic and nondiabetic control mice across a panel of 28 F1 mouse strains. Panel labels show correspondence with panels in Figures 1, 3–5. For each phenotype, strains are shown in alphabetical order by strain in order to facilitate trait‐trait comparisons across strains. Gray bars show control mice and black bars show diabetic mice. Error bars indicate SEM.
Mentions: Albuminuria, polyuria and blood urea nitrogen for diabetic and nondiabetic control mice across a panel of 28 F1 mouse strains. To test the impact of genetic background on traits associated with DN, DBA/2.Akita male mice were bred to females of 28 different inbred lines and the resulting male F1 animals were evaluated. F1 animals inheriting the Akita mutation are labeled as diabetic while offspring without the mutation are used as normoglycemic controls. The variation in genetic background as determined by the maternal strain is indicated on the horizontal axis for each graph. For each phenotype, strains are shown in rank order according to strain‐values for that phenotype in diabetic mice. Gray bars show control mice and black bars show diabetic mice. Error bars indicate SEM. (A) Albumin‐to‐creatinine ratios (ACRs, μg urinary albumin per mg urinary creatinine) varied widely among the strains and were elevated for diabetic versus nondiabetic controls in most cases (n = 4–17 mice/group). Nearly all strains showed significant increases in ACR with diabetes (P < 0.001–0.050). (B) Average urine volume (mL per 24 h). Severe polyuria is seen for diabetic as compared to nondiabetic mice. (C) Blood urea nitrogen (BUN) levels (mg/dL). *P < 0.05, n = 4–17. To facilitate comparisons among strains, these data are presented in alphabetical strain order in Figure 7‐1A, 1B and 1C at the end of the manuscript.

Bottom Line: 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.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.However, glomerular hypertrophy and collagen IV content were found to vary significantly among strains suggesting a genetic basis for early onset features of DN.

View Article: PubMed Central - PubMed

Affiliation: Division of Cardiology, Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California, USA.

No MeSH data available.


Related in: MedlinePlus