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Title: Increased renal hypertrophy in diabetic mice genetically modified at the haptoglobin locus
Authors: Miller-Lotan, R.
Herskowitz, Y.
Kalet-Litman, S.
Nakhoul, F.
Aronson, D.
Zoabi, R.
Asaf, R.
Ben-Izhak, O.
Sabo, E.
Lim, S.-K. 
Baumann, H.
Berger, F.G.
Levy, A.P.
Keywords: Diabetic vascular complications
Genetic susceptibility
Issue Date: Jul-2005
Citation: Miller-Lotan, R., Herskowitz, Y., Kalet-Litman, S., Nakhoul, F., Aronson, D., Zoabi, R., Asaf, R., Ben-Izhak, O., Sabo, E., Lim, S.-K., Baumann, H., Berger, F.G., Levy, A.P. (2005-07). Increased renal hypertrophy in diabetic mice genetically modified at the haptoglobin locus. Diabetes/Metabolism Research and Reviews 21 (4) : 332-337. ScholarBank@NUS Repository.
Abstract: Background: The human haptoglobin (Hp) gene is polymorphic with two functional classes of alleles, denoted 1 and 2. We have demonstrated in three longitudinal studies and several cross-sectional studies that the Hp genotype is an independent risk factor for diabetic vascular disease. These studies have presented a compelling argument that diabetic individuals homozygous for the Hp 1 allele are at decreased risk of vascular complications as compared to diabetic individuals with the Hp 2 allele. Methods: The naturally occurring (wild type) mouse Hp is a class 1 Hp allele. We examined renal hypertrophy in wild-type mice, Hp knockout mice (Hp 0), and in mice with the Hp 2 allele (Hp 2) with and without diabetes. Results: In the absence of diabetes, we found that renal hypertrophy was significantly increased in Hp 0 mice and that this could be prevented with vitamin E. There was no difference between wild type and Hp 2 mice with regard to renal hypertrophy in the absence of diabetes. However, in the presence of diabetes, Hp 2 mice demonstrated a significant increase in renal hypertrophy as compared to wild-type mice. Conclusions: These results support a direct linkage between diabetic vascular disease and the Hp genotype. These Hp-modified mice may serve as a platform on which to test a variety of pharmacological agents in order to decrease diabetic vascular disease. Copyright © 2005 John Wiley & Sons, Ltd.
Source Title: Diabetes/Metabolism Research and Reviews
ISSN: 15207552
DOI: 10.1002/dmrr.556
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