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Start Over Descriptor "Akita" Journal physiological reports
2 results on '"Akita"'

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

Author

Wu, Xiuju, Davis, Richard C., McMillen, Timothy S., Schaeffer, Valerie, Zhou, Zhiqiang, Qi, Hongxiu, Mazandarani, Parisa N., Alialy, Roshanak, Hudkins, Kelly L., Lusis, Aldons J., and LeBoeuf, Renée C.

Subjects
*DIABETIC nephropathies, *LABORATORY mice, *ALBUMINS, *CREATININE, *CYSTATINS, *BLOOD urea nitrogen
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. [ABSTRACT FROM AUTHOR]

Published
2014
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2. Genetic modulation of diabetic nephropathy among mouse strains with Ins2 Akita mutation

Author

Zhiqiang Zhou, Timothy S. McMillen, Kelly L. Hudkins, Aldons J. Lusis, Xiuju Wu, Roshanak Alialy, Richard C. Davis, Valerie Schaeffer, Renee C. LeBoeuf, Hongxiu Qi, and Parisa N. Mazandarani

Subjects
medicine.medical_specialty, Physiology, Renal function, 030209 endocrinology & metabolism, Diabetic nephropathy, medicine.disease_cause, 03 medical and health sciences, 0302 clinical medicine, Inbred strain, Physiology (medical), Diabetes mellitus, Internal medicine, medicine, Akita, Genetics, Albuminuria, Blood urea nitrogen, 030304 developmental biology, Original Research, 0303 health sciences, Mutation, biology, business.industry, medicine.disease, Animal models, Endocrinology, Cystatin C, biology.protein, medicine.symptom, business
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., Diabetic nephropathy (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 on different genetic backgrounds were evaluated for DN‐related traits and the results define the range of DN phenotypes that occur among common inbred strains of mice.

Published
2014

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