Abstract
Diabetic nephropathy is a major cause of end-stage renal failure (ESRF) in patients with both type 1 and type 2 diabetes. Many factors such as genetic and non-genetic promoters, hypertension, hyperglycemia, accumulation of advanced glycation end products (AGEs), dyslipidemia, albuminuria and proteinuria influence the progression of this desease. It is important to determine pathogenesis and treatment of this disease. However, it is difficult to investigate since human diabetes is a heterogeneous and multifactorial disease. Therefore, most of these mechanisms have been investigated in animal experiments. KK/Ta mice have a clearly different genetic background in terms of body weight, blood glucose, impaired glucose tolerance (IGT), urinary albumin excretion and serum triglyceride than BALB/c mice. Renal lesions of KK/Ta mice closely resemble those in human early diabetic nephropathy. Thus, the KK/Ta mouse may serve as a suitable model for the study of type 2 diabetes and early diabetic nephropathy in humans. We reviewed genetic susceptibility using genome-wide linkage analysis and differential display polymerase chain reaction (DD-PCR) or Northern blot analysis, and treatment of diabetic nephropathy using angiotensin type 1 (AT1) receptor blockers (ARB) or thiazolidinediones (TZDs) in KK/Ta mice.
Keywords: kk/ta mouse, diabetic nephropathy, gene, angiotensin type 1 receptor blockers (arb), thiazolidinediones (tzds)
Current Diabetes Reviews
Title: Pathogenesis and Treatment of Type 2 Diabetic Nephropathy: Lessons from the Spontaneous KK/Ta Mouse Model
Volume: 1 Issue: 3
Author(s): Yasuhiko Tomino, Mitsuo Tanimoto, Toshihide Shike, Kenji Shiina, Qiuling Fan, Jie Liao, Tomohito Gohda, Yuichiro Makita and Kazuhiko Funabiki
Affiliation:
Keywords: kk/ta mouse, diabetic nephropathy, gene, angiotensin type 1 receptor blockers (arb), thiazolidinediones (tzds)
Abstract: Diabetic nephropathy is a major cause of end-stage renal failure (ESRF) in patients with both type 1 and type 2 diabetes. Many factors such as genetic and non-genetic promoters, hypertension, hyperglycemia, accumulation of advanced glycation end products (AGEs), dyslipidemia, albuminuria and proteinuria influence the progression of this desease. It is important to determine pathogenesis and treatment of this disease. However, it is difficult to investigate since human diabetes is a heterogeneous and multifactorial disease. Therefore, most of these mechanisms have been investigated in animal experiments. KK/Ta mice have a clearly different genetic background in terms of body weight, blood glucose, impaired glucose tolerance (IGT), urinary albumin excretion and serum triglyceride than BALB/c mice. Renal lesions of KK/Ta mice closely resemble those in human early diabetic nephropathy. Thus, the KK/Ta mouse may serve as a suitable model for the study of type 2 diabetes and early diabetic nephropathy in humans. We reviewed genetic susceptibility using genome-wide linkage analysis and differential display polymerase chain reaction (DD-PCR) or Northern blot analysis, and treatment of diabetic nephropathy using angiotensin type 1 (AT1) receptor blockers (ARB) or thiazolidinediones (TZDs) in KK/Ta mice.
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Cite this article as:
Tomino Yasuhiko, Tanimoto Mitsuo, Shike Toshihide, Shiina Kenji, Fan Qiuling, Liao Jie, Gohda Tomohito, Makita Yuichiro and Funabiki Kazuhiko, Pathogenesis and Treatment of Type 2 Diabetic Nephropathy: Lessons from the Spontaneous KK/Ta Mouse Model, Current Diabetes Reviews 2005; 1 (3) . https://dx.doi.org/10.2174/157339905774574374
DOI https://dx.doi.org/10.2174/157339905774574374 |
Print ISSN 1573-3998 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-6417 |
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